Moderna Therapeutics has taken a major step forward in its efforts to produce a cancer vaccine based on the growing volume of research on messenger RNA (mRNA). The company has launched a study into the treatment’s effectiveness, administering the vaccine to its first human subject.
In recent years, the cost of sequencing the entire genome has fallen dramatically. Moderna is making full use of this ability when it comes to its potentially groundbreaking vaccine.
The company took a 1-millimeter cube of cancer tissue taken from the lung of the subject of the trial. Its genetic code was scanned and compared to a blood sample, which helped track down the changes that caused the cancer.
This information was used to produce a list of 20 protein targets that were tailored to the patient’s cancer. Scientists constructed DNA templates to make the necessary edits, then had them transcribed to RNA that would be administered via an injection.
“An individualized medicine designed to help each patient’s immune system better recognize cancer as foreign and attack it would be a critical addition to oncologists’ treatment arsenal, potentially helping many more patients respond more effectively to treatment,” said Howard A. “Skip” Burris III, MD, a principal investigator on the study, in a press release.
The idea of a cancer vaccine isn’t particularly new, but the capacity to produce treatments that are customized to a particular patient’s needs has come about relatively recently. Previous trials of a similar treatment have proven promising, so there’s plenty of reason to be optimistic about Moderna’s chances to create something truly remarkable.
That said, there are some important caveats. For one, there’s the questions of pricing – given how new this treatment is, and the fact that it has to be adapted to the individual, it’s likely that it will be very expensive. Moderna hasn’t yet announced what it expects to charge for the vaccine.
The company itself has also been subject to some criticism for an over-reliance on mRNA, described as a “one-size-fits-all” approach in a report from Bloomberg. Moderna specializes in using the molecules, which have shown to have significant potential, but the fact is that the technology is unproven. It can be difficult to prevent the immune system from killing them off.
Of course, there’s a long way to go before the vaccine is ready for widespread usage. For the time being, it’s being trialled with subjects who have already had their tumors removed. If the initial tests go well, then the sample will be expanded to include patients who have active cancer.
Up to 90 patients are expected to take part in the trial, which will yield initial results by the end of 2018.
It’s not every day that a group of the nation’s top cancer doctors asks people to curb their drinking.
In a statement released Tuesday, the American Society of Clinical Oncology outlined research tying alcohol to two types of cancer and told Americans to drink less.
“ASCO believes that a proactive stance by the Society to minimize excessive exposure to alcohol has important implications for cancer prevention,” the statement, which was published in the Journal of Clinical Oncology, said.
This is the first time the organization has taken a stance on alcohol and cancer, but it is not the first time that research has found strong links between the two.
This summer, two major research groups found strong evidence that drinking alcohol — as little as a glass of wine or beer a day — increases the risk of developing both pre- and postmenopausal breast cancer. For that report, scientists from the American Institute for Cancer Research and the World Cancer Research Fund looked at 119 studies from around the globe and incorporated data from roughly 12 million women as well as some 260,000 cases of breast cancer.
The US Department of Health and Human Services lists alcohol as a known human carcinogen. Research highlighted by the National Cancer Institute suggests that the more alcohol you drink — particularly the more you drink regularly — the higher your risk of developing cancer.
Still, before you pour out the wine in your cupboard, it’s important to keep in mind that the researchers are not saying every glass jacks up your chances of getting cancer.
“We’re not saying no one should ever drink at all — we’re just saying if you do drink, even trying to keep it down to less than one drink a day would be a smart choice,” Alice Bender, a registered dietitian who is the head of nutrition programs for the AICR, told Business Insider in May.
The researchers behind ASCO’s latest statement agree.
“The message is not, ‘Don’t drink.’ It’s, ‘If you want to reduce your cancer risk, drink less. And if you don’t drink, don’t start,’” Noelle LoConte, an associate professor at the University of Wisconsin at Madison who was the lead author of the ASCO statement, told The New York Times.
Alcohol is not the only important factor to consider when trying to reduce your cancer risk — your genes, exercise regimen, and exposure to pollutants can play a role, too.
The recent study also found, for example, that vigorous exercise was linked with a significant decrease in breast-cancer risk. The women in the studies who were the most active had a lower risk of developing cancer compared with those who exercised the least.
“It’s good to look at where you are with diet and physical activity and look at places where you might improve and just start every day to take some simple steps to decrease your risk and improve your health,” Bender said. “A little bit of change can make a real difference.”
Earlier this year, Microsoft launched Healthcare NExT, a new initiative that aims to bring together artificial intelligence, health research, and the expertise of its industry partners in order to provide people with the means to live healthier lives and cure deadly disease. In a blog post detailing the initiative, Microsoft noted how few other industries have the problems as complex as that of health care, though the company believes it can make headway by incorporating new innovative technology.
“It’s a big challenge,” said Peter Lee, Corporate Vice President at Microsoft Research NExT. “But we believe technology – specifically the cloud, AI and collaboration and business optimization tools – will be central to health care transformation.”
As reported by Digital Journal, Microsoft is expanding Healthcare NExT to cancer research in an effort to further work done to find a cure or effective treatment for the disease. However, it’s approaching cancer research as a tech company instead of a medical one — it sees living cells as something similar to computers, with diseases like cancer akin to glitches in the system. Extrapolated to this abstract point, this means Microsoft also views cancer cells as something that can be reprogrammed instead of destroyed; deleted instead of killed off.
Using Machine Learning to Improve Treatment
Microsoft’s cancer research is conducted at one of its biological computation labs in Cambridge, UK. Last year, a group of researches revealed their ongoing work to develop a computer system that would live inside human cells and restart the system if cancer cells were detected, thereby cleaning out the afflicted cells. Other projects included using machine learning to improve tumor scanning, to better organize patient data, and to discover better treatments.
“If you look at the combination of things that Microsoft does really well, then it makes perfect sense for Microsoft to be in this industry,” said Andrew Phillips, head of the biological computation research group at Microsoft’s Cambridge lab, in a Microsoft Story Labs post. “We can use methods that we’ve developed for programming computers to program biology, and then unlock even more applications and even better treatments.”
Discovering a cure for cancer is an ambitious goal to take on, and it remains to be seen how cancer research will be improved with Microsoft’s involvement. That said, Microsoft has expressed a desire to “empower every person and organization to achieve more.” If it can maintain that drive and focus, who knows what the company will develop.
“We are incredibly energized about the opportunities to make a difference in health care,” said Microsoft. “We’ve been listening carefully to our customers and partners within the health care sector, and we’ve heard their message: Let’s work together, innovate together and create solutions that can empower people to lead healthier lives.”
The aging process is a constant in life that binds every single living creature on the planet – and for generations, there have been those who dedicate their lives to fighting it. However, a new study suggests that it’s mathematically impossible to deny the ravages of age in a multicellular organism.
One popular theory outlines a method that could potentially stop aging by taking advantage of natural selection. It’s been hypothesized that if the body’s healthy cells are preserved while less capable cells linked to aging were removed from the equation, humans could remain youthful indefinitely.
Unfortunately, this new study asserts that this isn’t the case. Even if the body could be trained to get rid of cells that become sluggish and lose their functionality, there are certain cells that reproduce at a higher rate among older people, which leads to an increased risk of cancer.
The researchers state that all of us will develop cancer cells at some point in our lives, even if we never display any symptoms. The problem here is that these cells don’t play fair when it comes to natural selection.
“As you age, most of your cells are ratcheting down and losing function, and they stop growing, as well,” said Paul Nelson, the lead author of the study, in a press release. “But some of your cells are growing like crazy. What we show is that this forms a double bind – a catch-22. If you get rid of those poorly functioning, sluggish cells, then that allows cancer cells to proliferate, and if you get rid of, or slow down, those cancer cells, then that allows sluggish cells to accumulate. So you’re stuck between allowing these sluggish cells to accumulate or allowing cancer cells to proliferate, and if you do one you can’t do the other.”
With Age Comes Wisdom
According to this study, growing old is an inescapable tenet of life as a multicellular organism. However, a variety of ongoing projects are still actively seeking a way to dodge the effects of time.
However, if the aging process really is a decision between slowing cells or multiplying cancer cells, these treatments might prove to be unsuccessful in practice. Solving one problem may simply leave the body open to another form of degradation.
It may well be that our best method of dodging the aging process is to abandon our organic form altogether. If we’re doomed to fall apart on a cellular level, turning to technology might be our best bet for an expanded lifespan. A mechanical body wouldn’t be subject to the same constraints as flesh and bone. Of course, the biggest challenge in this hypothetical transformation would be transferring our consciousness to some kind of synthetic platform so that we could truly free ourselves from the limitations of organic matter. However, surprisingly, this idea is not as outlandish as it may seem.
A new computer-aided endoscopic system that probes for signs of tumor or cancer growth in the colon may very well be the future of cancer detection. Assisted by artificial intelligence (AI), the new diagnostic system is able to tell if clumps of cells, called colorectal polyps, that grow along the walls of the colon are benign tumors known as colorectal adenoma.
The computer-assisted diagnostic system was trained using more than 30,000 images of colorectal polyps, each magnified 500-times, and operates using machine learning. The AI can check approximately 300 features of the polyp, which it compares to its existing “knowledge”, in less than a second. After having been used successful in preliminary studies, prospective trials followed. The results of these trials, the first for AI-assisted endoscopy in a clinical setting, were presented at the 25th UEG Week in Barcelona, Spain.
The prospective study was conducted by a team led by Dr. Yuichi Mori from Showa University in Yokohama, Japan. Mori and his colleagues tested the new system in 250 patients previously identified to have colorectal polyps. The AI predicted the pathology of each polyp, comparing it with final pathological reports taken from the resected specimens. The results were highly encouraging — the system assessed 306 polyps in real-time, with a 94 percent sensitivity, 79 percent specificity, and 86 percent accuracy. In identifying abnormal tissue growth, the system demonstrated 79 percent positive and 93 percent negative predictive values.
AI in Healthcare
In short, the AI was able to fairly accurately identify which abnormal colon cell growths were most likely to be cancerous. “The most remarkable breakthrough with this system is that artificial intelligence enables real-time optical biopsy of colorectal polyps during colonoscopy, regardless of the endoscopists’ skill,” Mori said, speaking during the Opening Plenary at the UEG Week. “This allows the complete resection of adenomatous polyps and prevents unnecessary polypectomy of non-neoplastic polyps.”
Furthermore, the researchers presented the results of their prospective study to prove that their system was ready for clinical trials.”We believe these results are acceptable for clinical application and our immediate goal is to obtain regulatory approval for the diagnostic system,” Mori added.
Moving forward, Mori’s team plans to conduct a multicenter study to aid eventual clinical tests. They’re also working on an automatic polyp detection system. “Precise on-site identification of adenomas during colonoscopy contributes to the complete resection of neoplastic lesions” said Dr Mori. “This is thought to decrease the risk of colorectal cancer and, ultimately, cancer-related death.”
A new study has established that RNA molecules, originally developed as a means of studying genes, can trigger a hidden mechanism that prompts cells to commit suicide. Some scientists believe that this could be used as a new method of cancer treatment.
“It’s like committing suicide by stabbing yourself, shooting yourself and jumping off a building all at the same time,” said lead study author Marcus Peter in a statement published via the Northwestern University website. “You cannot survive.”
Peter and his team found sequences in the human genome that possess this capability when converted into small double-stranded RNA molecules. It’s thought that the mechanism is an ancient technique that cells used to eliminate cancer before the advent of the adaptive immune system, many millions of years ago.
Cells have been fighting cancer since life became multicellular, so Peter felt confident that there had to be a “fail-safe” that could combat it as soon as it began to take hold. However, identifying and finding these particular molecules was very difficult, as they would only be active at the precise moment that the cell became cancerous.
Peter found that small interfering RNAs were capable of killing cancer cells, as well as fulfilling their intended purpose of suppressing gene activity. All the genes necessary for cell survival are eliminated, with very little effect on normal cells.
Urology professor Dr. Shad Thaxton collaborated with Peter to test whether this mechanism could be used as a cancer treatment. Nanoparticles were used to administer the molecules to mice bearing human ovarian cancer, which slowed the growth of tumors without raising the animals’ toxicity levels. Crucially, the tumors did not develop a resistance to this treatment.
Cancer survival rates are more promising than ever before because of significant advances in diagnosis. However, we’ve made less progress when it comes to treatment methods.
“If you had an aggressive, metastasizing form of the disease 50 years ago, you were busted back then and you are still busted today,” said Peter. “Improvements are often due to better detection methods and not to better treatments.”
Immune therapy has proven to be very effective, but only a select subset of cancers respond to the treatment. Peter draws a comparison between the methods established by this study and immune therapy because both utilize natural mechanisms taken from the evolutionary process.
“Our research may be tapping into one of nature’s original kill switches, and we hope the impact will affect many cancers,” said Peter. “Our findings could be disruptive.”
Over the years, scientists have dedication innumerable time, energy, and resources to cancer research in an attempt to discover — or develop — cures. One of the most notable observations science has made comes from cancer’s relationship with sugar. While the extent to which the two relate has previously been unidentifiable, a new study sheds light on the relationship.
Referred to as the Warburg effect, we know cancer (not unlike the human body) needs sugar for energy and to promote growth. The amount of sugar the cancerous cells require, however, is much higher than what healthy cells need — as is the rate at which cancer cells turn sugar in lactic acid.
Due to the nature of the Warburg effect, it’s been difficult to firmly establish whether it is a contributing cause of cancer, or the result of it. The latest study, the result of a nine-year long research project, has provided new insights about the metabolic process, revealing that it does, indeed, stimulate the creation of cancerous tumors.
“Our research reveals how the hyperactive sugar consumption of cancerous cells leads to a vicious cycle of continued stimulation of cancer development and growth,” said researcher and Prof. Johan Thevelein from KU Leuven in Belgium. “Thus, it is able to explain the correlation between the strength of the Warburg effect and tumor aggressiveness.”
Thevelein and his team used yeast to conduct their research, as yeast contains the same ‘Ras’ proteins found in cancer cells. It also has a highly active sugar metabolism. The team observed that the introduction of a large amount of sugar caused the Ras proteins to overreact, leading to an increased amount of yeast and cancer cells created.
“It is striking that this mechanism has been conserved throughout the long evolution of yeast cell to human,” added Thevelein.
In any case, the research done by Thevelein and his team, published in the journal Nature Communications, makes such a treatment slightly more plausible. Thevelein said the team’s work will “provide a foundation for future research in this domain, which can now be performed with a much more precise and relevant focus.”
The research did not, however, offer an explanation regarding the cause of the Warburg effect. Additional research would be required to establish the phenomenon’s cause.
New research has shown that cancer cells that survive treatment may effectively wake themselves up and resume growing by tapping into the body’s immune system as a power source. This work provides more insight into the puzzle of why, and how, cancer relapses, and has provided key insights into why the immune system may fail to fight cancer effectively. The research also revealed that, by restoring the body’s immune response to proper functioning, immunotherapy might prove effective at preventing relapse of the deadly disease.
The research question for this team was how a relatively tiny number of treatment-resistant cancer cells could become a deadly occupying force after remaining dormant for stretches of time. In an attempt to answer this question, the team studied immune responses in mice. They were watching to see how immune system cells operate before treatment for cancer, after treatment was declared a success, and once tumors returned.
Normally, immune cells trigger inflammation by releasing signals when they sense infection or trauma. This can, in some cases, help the immune system kill cancer cells. However, post-treatment cancer cells subvert these signals. In the study, researchers targeted the response to the post-treatment cells using immunotherapies, and were able to delay — or in some cases prevent — relapse.
The key discovery was that a chemical signal called TNF-alpha can switch roles: it can either serve as an anti-tumor agent, supporting the immune response to cancer cells, or as a new type of relapse promoting signal. TNF-alpha was also able to trigger the resistant cells, prompting them to influence cells that kill cancer naturally not to attack.
Cells Ignoring the Problem
Specifically, the team found that the surfaces of resistant cancer cells had high levels of a certain molecule, PD-L1, on their surface. The PD-L1 on those cells can act with other PD-L1 on T cells, instructing them to ignore signals. These results suggest that, after surviving treatment, cancer cells wake themselves up and start growing again using the patient’s immune system. Once this mechanism is better understood, immunotherapy could provide potential treatment for humans. As such, this is the next area of research the team plans to pursue.
“Our study finds the body’s own immune system seems to play a crucial role when cancer relapses,” co-author Professor Alan Melcher said in a press release. “The immune system goes from keeping cancer cells in check to awakening and feeding residual cells, while turning a blind eye to their growth.”
“Excitingly, many of the methods employed by treatment-resistant tumours to re-grow and hide from the immune system can be blocked using existing immunotherapies.” The researchers also added that, based on recent supporting data from clinical trials, the potential of immunotherapy to reduce cancer relapse is good.
Co-author Kevin Harrington added: “It is becoming increasingly clear that the immune system is at the core of the puzzle of how we can treat cancer more effectively.”
Genetically Engineered Eggs are Better than Golden Eggs
People often warn about the amount of cholesterol you get from eating too many eggs. But what if there were health benefits to eggs as well — like drugs that fight cancer, hepatitis, and other diseases? Japanese researchers from the National Institute of Advanced Industrial Science and Technology (AIST) did just that when they successfully genetically engineered chickens to lay eggs that contain a special pharmaceutical agent.
According to a report by The Japan News, the researchers at AIST genetically modified precursor cells of chicken sperm to produce a type of protein that’s related to the immune system called interferon beta.
This protein has been found to be effective in treating malignant skin cancer and hepatitis. The modified cells were used to fertilize eggs that produced male chicks. A few rounds of cross-breeding the male chicks resulted in chickens that inherited the genes with interferon beta.
Reagent import and sales firm Cosmo Bio Co. in Tokyo, which developed the method together with the AIST researchers and the the National Agriculture and Food Research Organization in Ibaraki Prefecture, now has three hens that lay eggs every one or two day. The egg whites from those eggs contain interferon beta.
Why go through such a tedious process? The project’s goal was to potentially reduce the costs of making drugs. “This is a result that we hope leads to the development of cheap drugs,” Hironobu Hojo, professor at Osaka University, told The Japan News. “In the future, it will be necessary to closely examine the characteristics of the agents contained in the eggs and determine their safety as pharmaceutical products.”
This is just one example of how gene editing methods can reshape industries, especially healthcare. Others have worked on applying gene editing such as CRISPR directly into cancer cells or to a patient. Producing cheap drugs from chicken eggs is another possibility — and a rather creative one, at that.
Moving forward, the researchers plan to work on stabilizing the interferon beta contents of the eggs to produce some a dozen milligrams to 100 milligrams from a single egg.
A team of researchers has developed a method of using virtual reality headsets to view 3D models of genetic data. The simulations bring together data from genome sequencing, information about DNA interactions, and microscopy data.
“By combining data on the genome sequence with data on gene interactions we can create a 3-D model that shows where regulatory elements and the genes they control sit relative to each other,” said Prof. Jim Hughes, Associate Professor of Genome Biology at Oxford University, in a press release. “It makes it easier to understand the processes going on within a living cell.”
Each of the 37 trillion cells in an adult human body holds two meters of DNA within its nucleus. We’ve had the capability to sequence DNA for a long time, but the way the two-mile strand of DNA is folded up might directly influence gene expression. If we can visualize the specific arrangement, we might be more effective at finding important insights into human genetic disease, because humans are very good at visual pattern recognition.
The researchers are currently using this visualization technique to study diabetes, cancer, and multiple sclerosis. The long-term goal is for the project to help with efforts to establish a method of correcting faulty genes and introducing them to the body.
Since 2011, researchers have been conducting clinical trials involving a modified type of poliovirus as a form of treatment against recurrent glioblastoma — a very aggressive kind of brain tumor. The promising results of these trials prompted researchers from the Duke Cancer Institute to look into the deeper mechanisms behind the treatment, and the results of their study have now been published in Science Translational Medicine.
Led by Matthias Gromeier and Smita Nair, the research team studied the impact of introducing the modified virus, known as a recombinant oncolytic poliovirus (PVS-RIPO), to two human cancer cell lines: melanoma and triple-negative breast cancer.
They learned that the CD155 proteins produced by the cancer cells acted as receptors for the poliovirus. Once attached to the cancer cells, the virus began to attack them, causing the tumor to produce antigens. These antigens then triggered an immune response from the body, which began attacking the malignant cells.
In addition to attacking the cancer cells, PVS-RIPO also infected the immune system’s dendritic cells and macrophages. The former are tasked with processing antigens in a way that brings them to the attention of T-cells, thus triggering their defensive response. Once these dendritic cells were infected by PVS-RIPO, the T-cells knew to begin attacking the tumor.
The results of the researchers’ tests were later on validated on mouse models in the lab.
While the results of the clinical trials already suggested that PVS-RIPO was a promising new treatment option, the Duke team’s research adds an entirely new dimension to its potential as a weapon against cancer.
“Not only is poliovirus killing tumor cells, it is also infecting the antigen-presenting cells, which allows them to function in such a way that they can now raise a T-cell response that can recognize and infiltrate a tumor,” Nair explained in a press release. “This is an encouraging finding, because it means the poliovirus stimulates an innate inflammatory response.”
In short, this modified poliovirus is able to create a cell culture that’s harmful to cancer cells, and it does so in tandem with mechanisms already present in the human body. “This is hugely important to us,” said Gromeier. “Knowing the steps that occur to generate an immune response will enable us to rationally decide whether and what other therapies make sense in combination with poliovirus to improve patient survival.”
To that end, the Duke researchers think that their study warrants pushing clinical trials to the next level. “Our findings provide clear rationales for moving forward with clinical trials in breast cancer, prostate cancer, and malignant melanoma,” Gromeier told Medical News Today. “This includes novel combination treatments that we will pursue.”
The Warburg Effect refers to the way cancer cells “rewire” their metabolism to survive, voraciously consuming glucose to produce energy. Although scientists have known about this process for decades, they have not yet been able to harness it to stunt tumor growth. However, new research out of the Duke Cancer Institute may be able to change that.
In a study published today in Cell Metabolism, researchers detail how they were able to interpret the unusual wiring system that cancer cells use to metabolize carbohydrates, as well as identify a natural compound that shuts the system down selectively, at least in the lab.
Whereas healthy cells break down sugar with oxygen, cancer cells use fermentation, a less efficient process that requires more sugar, so the researchers began by studying cancer cells to better understand how their metabolism differs from that of normal cells.
Next, the team observed cancer cells undergoing the Warburg Effect to determine specific points where the cells controlled carbohydrate metabolism differently than their healthy cell counterparts.
The researchers found that the enzyme GAPDH controls the rate of glucose processing in cancer cells, so they then searched for any compounds known to have the potential to block the GAPDH enzyme. They saw potential in koningic acid (KA), a molecule that’s produced by a sugar-eating fungus to prevent bacteria from honing in on its food supply.
Based on their suspicions that it might naturally target the cells engaged in accelerated glucose metabolism, the team tested KA in cancer cells and mouse models. The results of these tests indicate that KA does curb glucose consumption in tumors undergoing the Warburg Effect by selectively inhibiting the GAPDH enzyme, all while leaving normal cells alone.
The Warburg Effect is strong in some cancers, but weak or even absent in others. During the course of their study, the Duke researchers found that they could develop a model to predict the extent to which a cell would be under the influence of the Warburg Effect by measuring its GAPDH enzyme. These models could make it easier to predict when a therapy that targets the metabolic process is most likely to have the biggest effect.
“We’ve seen with genetics that cancers can be targeted based on whether certain mutations are present, and it could be that selectively targeting tumors based on their metabolism could have a similar impact,” lead author Maria Liberti said in a press release.
The team believes their results demand further study, specifically to determine whether other molecules might work along the same pathway and whether KA’s effects can be reproduced in other cell and animal studies.
“These findings not only show that KA’s efficacy is linked to the quantitative extent of the Warburg Effect, but that this also provides a therapeutic window,” explained Jason Locasale, the paper’s senior author and an assistant professor at Duke’s Department of Pharmacology & Cancer Biology. “This could provide another way to attack cancer beyond the genetic makeup of the tumor. That’s encouraging.”
Cancer is, without a doubt, one of the most dreaded diagnoses a person can receive in their lifetime. While there are many forms of cancer and their respective prognosis depend on a multitude of factors — such as the patient, the cancer’s stage, and available treatments — for the millions of people who will be diagnosed this year, the word “cancer” is still a frightening one to hear.
The American Cancer Society projected that 1,688,780 new cancer cases will be diagnosed in 2017. People of all ages can be among those diagnosed with one of over 100 different types of cancer. But when we talk about cancer — especially when we discuss treatments or cures — it’s important to point out that cancer is not just one disease. Therefore, the likelihood that a single treatment could ever cure all forms of cancer is extremely unlikely.
To frame the search for a cancer cure as being the quest for a single drug or procedure is approaching the task from within the wrong framework. Rather than developing a single cancer cure-all, many doctors are advocating that we focus instead on developing treatments that are disease-specific — and even patient-specific. This strategy is necessary because cancer can arise in different body systems, often several at the same time, and in different people with their own unique physiology.
Will such treatments ever exist? When it came to making predictions about when — if ever — we’ll have a cure for all forms of cancer, Futurism readers were pretty optimistic: 25 percent think we’ll get there by the 2030s, 18 percent by the 2040s, and 16 percent think we’re right on the cusp — predicting a cure as soon as the next decade. About 10 percent of readers predicted that we’ll never cure cancer.
Bård Pedersen, a reader from Norway, commented “I do actually think that it will be possible in the 2020s … But due to paperwork, testing en [sic] other legalities it will not be available as legal treatment until mid 2030s.” While Pedersen was commenting on the situation where he lives in Norway, approval for new drug treatments is an arduous process around the world. In the U.S., regulation is especially tight and can pose challenges for researchers, medical professionals, and patients alike.
While developing many different and even personalized treatments may seem like a lofty task, it’s actually something we have done and are doing. CRISPR has allowed researchers to edit a mouse’s genome such that their immune cells are genetically engineered to kill cancer cells. The clinical trials that have been completed thus far indicate it may be a good treatment option for patients with a form of cancer called multiple myeloma, a form of cancer that affects blood plasma cells.
Another mouse study that the University of Pittsburgh School of Medicine published earlier this year used genetic engineering to target cancer fusion cells — something that had never been done before. “It is really exciting because it lays the groundwork for what could become a totally new approach to treating cancer,” said the study’s lead author Jian-Hua Luo, director at Pitt’s School of Medicine’s High Throughput Genome Center, in a press release. These fusion genes — two genes that fuse together and produce cancer-promoting proteins — may play an instrumental role in many types of cancer.
What the Experts Say
While this research is promising, many cancer experts are still cautious about the future of the field. Monica Bertagnolli, chair of the Alliance for Clinical Trials in Oncology, told Scientific American last year that even if new treatments are developed and pass through the required regulatory hurdles, it still doesn’t mean they’ll work for every patient.
“Unfortunately, we see some patients don’t respond to these wonderfully new therapies and some patients that do respond initially eventually develop resistance to those therapies and so the tumor returns,” Bertagnolli said in the interview. “Obviously that’s in the way of curing cancer because we want a treatment that a patient will never develop resistance to.”
Other experts who have devoted their careers to cancer research — like Barrie Bode, biology chair at Northern Illinois University — acknowledge that there are many possibilities in research to be excited about, but haven’t become so caught up in the excitement that they lose sight of the reality. When asked if he thinks there will be a cure for cancer in our lifetimes, Bode said no, but added that “Some types of cancer might be cured — that’s happened already. But new pharmaceutical cures are rare. Over the next century, I’d say the chance is very remote that we will find a single ‘cure for cancer.’”
Bode’s commentary echoes that of many others, but that isn’t to say he’s entirely without faith that we’ll continue to make steady progress both in our understanding of cancer and developing more effective treatments. The search for a cure may not be as vital in the years to come as the commitment to developing treatment that can increase a patient’s quality of life, if not their life expectancy, too. Bode says treatments to come will be “informed by the science and technologies that are available so that cancer can be managed much like other diseases, such as heart disease and diabetes.”
If groundbreaking research and clinical trials are to continue, it will need funding. The Cancer Moonshot initiative, which was put into place under former President Obama and has former Vice President Joe Biden at the helm, was allotted $1.8 billion by Congress in December of 2016, to be used for the next seven years. Many goals of the program are focused on the outcome for cancer patients that is the closest we have to a cure: remission. While cancer that has gone into remission can come back, over the last few decades research has allowed patients with many forms of cancer to live long by extending their periods of remission through treatment.
See all of the Futurism predictions and make your own predictions here.
Cancer is nothing to mess around with. While alternative treatments may seem appealing to patients, some have been found to have more harmful effects in the aftermath.
Skyler Johnson and his colleagues at the Yale School of Medicine in Connecticut discovered this very fact when they decided to look into cancer treatments and cancer survivors. Records from the US National Cancer Database provided data on 281 people who tested positive for four types of cancer — lung, breast, prostate, or colorectal — and sought out alternative methods to deal with the disease, instead of the more conventional and often recommended treatments like chemotherapy, radiotherapy, or surgery.
“[These alternative treatments] could be herbs, botanicals, homeopathy, special diets or energy crystals, which are basically just stones that people believe have healing powers,” said Johnson.
Johnson doesn’t know specifically what treatments this group used, but his team’s results are telling.
Johnson and his team compared the aforementioned 281 people to 560 others of similar ages and race who also had cancer, but chose the conventional route. The alternative treatment group was two and half times more likely to die within five years of being diagnosed. That said, Johnson notes that the nature of prostate cancer makes the comparison a little inaccurate, since it takes longer for this specific form of the disease to progress to the point of becoming life-threatening.
Among breast cancer patients, specifically, those that chose alternate treatment were over five times more like to die within the same span of time. Forty-one percent of lung cancer patients who took conventional treatments survived at least five years, compared to 20 percent of those who eschewed the treatment in favor of alternatives. Only 33 percent of colorectal cancer patients survived five years following alternative treatments; 79 percent survived five years using recommended means.
Those Who Chose
Interestingly enough, those that decided to try alternative treatments were also people who were considered wealthy or well educated. Alternate treatments like herbs or diets can often be expensive, especially when offered by a large company.
“It’s a multibillion dollar industry. People pay more out-of-pocket for alternative treatments than they do for standard treatments,” John Bridgewater, an oncologist at the University College London Hospital, told New Scientist.
There’s nothing to prove these method work or do not work, however, making it hard to keep people from seeking them out. The fact that people sometimes survive the treatment can also make it difficult to condemn it, though Johnson has speculated they managed to do so because they eventually got the necessary treatments. Secondary treatments are not kept on record, so there’s no official way to tell if this was the case, or if instead the person was incredibly fortunate.
Alternative cancer treatments might sound appealing when compared to methods like chemotherapy, which can have frankly unpleasant side effects. Yet the fact remains that these methods have gone through rigorous scientific testing and peer review, which confers some degree of safety and effectiveness. The scientific process is far from perfect — but it’s still the best we’ve got.
Around three quarters of HPV infections are caused by just two of the nearly 200 strains of the virus: HPV 16 and HPV 18. Gardasil, the quadrivalent HPV vaccine that’s currently approved for use in Australia, protects against both of these forms.
During their study, which is published in the International Journal of Cancer, the researchers found that 77 percent of the 847 cervical cancer samples tested were caused by HPV 16 and 18. A further 16 percent were linked to HPV 31, 33, 45, 52, and 58. Gardasil 9, an HPV vaccine that was approved for use in the U.S. in 2014, protects against all seven of these strains.
Stamping Out Cancer
Based on these numbers, the researchers believe the Gardasil 9 vaccine could prevent up to 93 percent of cervical cancer cases.
“The new vaccine still protects against genital warts but is expanded to cover the seven most common viral types that cause cervical cancer,” said the senior author of the paper, Professor Suzanne Garland, in a Royal Women’s Hospital news release. “I do believe that if we continue with this high coverage of vaccination, we could almost wipe out cervical cancer in women.”
With the promising results of the study in hand, the next step is to ensure that as many people as possible have access to the Gardasil 9 vaccine. The Royal Women’s Hospital is hopeful that it will be adopted by Australia’s National HPV Vaccination Program as early as 2018.
Of course, to remove the threat of HPV causing cervical cancer completely, a vaccine would have to protect against the less common strains of HPV that comprise the remaining 7 percent of cases covered by this study. It remains to be seen how feasible that would be, but the extra coverage achieved by Gardasil 9 is definitely a big step forward.
Cancer is one of the leading causes of death worldwide, according to the World Health Organization, claiming 8.8 million victims in 2015. While researchers have made significant progress in the battle against the disease, it remains notoriously difficult to treat. This is due, in part, to the wide variety of cancers known to exist today, but the matter is further complicated by our difficulty preventing cancer cells from spreading.
While treatments such as chemotherapy and immunotherapy are available, they are often rendered ineffective by the fast rate at which cancer cells spread. Now, researchers from the University of Southampton in the United Kingdom, working in partnership with Cancer Research UK, may have found a way to aid such treatments by slowing down the spread of many different types of cancer.
In a study published in the Journal of the National Cancer Institute, the researchers focused on the enzyme NOX4 and a kind of cell called cancer associated fibroblasts (CAFs). When healthy, fibroblasts keep different kinds of organs together. When infected by cancer and turned into CAFs, however, they are known to help tumors grow, spread, and even evade treatment.
“By looking at many types of cancer, we have identified a common mechanism responsible for CAF formation in tumors,” lead research Gareth Thomas said in a press release. “These cells make cancers aggressive and difficult to treat, and we can see exciting possibilities for targeting CAFs in many patients who don’t respond well to existing therapies.”
The researchers found that CAFs decrease patient survival for a number of cancer types, including head, neck, and bowel cancers. “[E]ffective methods to manipulate these cells clinically have yet to be developed,” the researchers wrote. Thankfully, through their research, they discovered that NOX4 and CAFs have a peculiar dynamic.
In many types of cancer, NOX4 enzymes are required for CAFs to form and subsequently facilitate tumor growth. In tests conducted on mice, blocking NOX4 reduced the size of tumors by up to 50 percent. This blocking was made possible using a drug that’s being developed to treat another kind of disease called organ fibrosis.
“Some cancers are incredibly difficult to treat and can use the body’s own cells to help them grow, evade treatment, and spread around the body,” explained Áine McCarthy at Cancer Research UK in the press release. “Researchers have been trying to unlock the secrets behind this for many years, and this study is a big step forward in understanding how some cancers achieve this.”
“These findings show that CAFs can be targeted with a drug and their ‘pro-tumor’ effects can be reversed in mice, giving researchers a starting point to develop new and potentially more effective treatments in the future,” she added.
Thomas and his team believe that their work could help improve a patient’s chances of reacting positively to chemo and immunotherapy. At the very least, it could help slow down the spread of cancer, dealing a critical blow to the disease that affects so many people.
Scientists have come up with a potential new way to treat neuroblastoma, the most common kind of cancer in infants, by targeting it with nanoparticles loaded up with an ingredient of the spice turmeric.
Turmeric is more often used to add flavour to curries, but the curcumin chemical it contains has shown promising progress in tests in destroying neuroblastoma tumour cells resistant to other drugs.
If scientists can work out how to adapt this into a full and safe treatment, it would have the benefit of being less toxic and unpleasant for patients than traditional alternatives like chemotherapy – which is especially important when you’re dealing with young kids.
“High-risk neuroblastoma can be resistant to traditional therapy, and survival can be poor,” says lead researcher Tamarah J. Westmoreland, from the University of Central Florida.
“This research demonstrates a novel method of treating this tumour without the toxicity of aggressive therapy that can also have late effects on the patient’s health.”
Using curcumin to fight cancer isn’t a new idea, but it’s difficult to get the chemical into drugs because of its low solubility and poor stability. Nanoparticles could fix that.
During the study, cerium oxide nanoparticles loaded with curcumin and coated in dextran were shown to cause “substantial” cell death in neuroblastoma cells while having little impact on healthy cells – the perfect combination for a cancer drug.
Even better, the nanoparticles were more effective against the type of cells usually most resistant to conventional drugs, those with an amplification of the MYCN gene.
As neuroblastoma is usually very difficult to treat, that’s a promising start for these spicy nanoparticles. This type of cancer normally takes root near the kidneys, striking 700 people per year in the US, most of whom are under 5.
Not only is it largely resistant to anti-cancer drugs, it’s also known to cause health problems after successful treatment, including hearing loss and other disabilities. It also often returns after treatment.
If we can develop an effective nanoparticle approach to fighting neuroblastoma, it would be yet more evidence of the potential of treating disease at the smallest possible scales: nanoparticles have previously been shown to help kickstart the human immune system to help fight cancer, for example.
Other recent research has looked at how nanoparticles can better target tumours in the brain by squeezing through the blood-brain membrane barrier, as well as reaching other places that conventional drugs can’t get to.
The next step for the researchers behind the latest study is to see if the same positive effects can be observed in animal trials as well as lab tests.
“We are hopeful that in the future, nanoparticles can be utilised to personalise care to patients and reduce the late effects of therapy,” says Westmoreland.
Cancer comes in all shapes and sizes. It can affect any and every part of the human body in a variety of potentially debilitating — and even life-threatening — ways. So, while the vaccines developed as part of two recent studies published in the journal Naturecould lead to a whole new age of groundbreaking cancer therapies and treatments, they are by no means a “cure” for all the different forms of cancer.
Even still, these new vaccines are remarkable. While these vaccines are new, cancer vaccines in general are not. The researchers explored the possibility of creating vaccines personalized to an individual’s unique cancer mutations in order to combat tumors. The two clinical trials run thus far were small: in them, the researchers attempted to design individual vaccines in hopes they would give the patient the ability to fight off tumors in a way optimized for their biology. These studies also briefly noted the potential to combine such vaccines with existing immunotherapies to give the body an increased chance of combatting a cancer’s spread.
In a basic sense, these vaccines are cancer cells combined with immune system stimulating agents. It’s not unlike how flu vaccines combine virus with ingredients designed to ignite a particular immune response. The research team in these trials hoped the vaccines would enable the patient’s immune system to attack the cancer cells.
In the first of two clinical trials, 4 out of the 6 patients hadn’t seen their tumors return. The remaining 2 eventually went into complete remission with additional treatment. In the second trial, 8 out of 13 total patients remained tumor free more than a year after the study. In the remaining 5, their tumors had spread already by the time they received the vaccine — but two of their tumors did shrink. Another 5 went into complete remission after receiving additional treatment.
According to Cornelis Melief, a cancer immunologist at Leiden University Medical Centre in the Netherlands who authored a commentary on the study, “It’s potentially a game changer…The two papers really strongly indicate that the patients experienced clinical benefit.”
The Future of Treatment
As previously stated, only two small clinical trials have been completed so far. These personalized vaccines might seem like our greatest weapon yet in battling tumors, but these studies are just the beginning. While the results seem promising — and certainly very exciting — they are not a direct indicator for success. Additional research and trials will need to be conducted before the idea of cancer vaccines could be implemented on a larger scale.
However, if the direction of these studies continues to trend in this way, cancer treatment could be forever changed. Not only would the vaccine be capable of being personalized and specified for an individual’s biology and specific mutations, it could be tailored for the type of cancer as well. And, the more we can individualize treatment, it seems, the better chance we will have of giving every cancer patient the very best shot at remission.
The growing number of people who have the disease is troubling, because there are only four approved drugs that treat symptoms of the disease, and several hopeful treatments have failed key studies in 2017.
Unexpectedly, it’s something researchers at the top cancer hospital in the US are looking into. While cancer and Alzheimer’s seemingly don’t have that much in common, there is one key link that researchers at MD Anderson think could be useful: People with a history of cancer are less likely to get Alzheimer’s, while people with Alzheimer’s are less likely to get cancer.
“Age is the biggest risk factor for both. But then for some reason, some people go one direction, others go another direction,” Jim Ray, head of research for the Neurodegeneration Consortium at MD Anderson told Business Insider.
In the last decade the researchers have made this observational link between the development of Alzheimer’s and a decreased cancer risk and vice versa. So researchers have been hypothesizing why that happens. At a very simplified level, the cause of the diseases might hold the biggest clue. “Cancer is a disease of cells that cannot die, will not die. Alzheimer’s is a disease of cells that are supposed to live your entire lifetime that you can’t keep alive,” he said.
One of the ways researchers have been getting clues into the link is in cancer patients who have chemotherapy-related cognitive dysfunction. An estimated 75% of cancer patients have some level of cognitive impairment (memory loss, attention problems, etc.). Chemotherapy works by killing cancer cells by targeting fast-dividing cells, and in most cases, kills off some healthy cells along the way, including nerve cells in the brain.
“It’s an understudied area,” Ray said. “And I think a lot of people didn’t fully realize it was a problem.”
It’s something drug researchers have started looking into, to see if there could be a therapy that prevents the neurological damage that happens with chemotherapy. If they can figure out what’s going on and how to prevent the neurological side effects for cancer patients, the same approach could hold some promise in treating Alzheimer’s as well.
New Ways to Tackle Alzheimer’s
The search for new Alzheimer’s treatments hasn’t been going well. The last new drug approved was back in 2003, and a slew of failed trials in the beginning of 2017 has cast a shadow over the field.
Still, more drugs are in late-stage trials that could have an impact on the disease, and researchers are pinning hopes on diagnosing the disease early, before symptoms even show up. If any of those treatments pan out, it could change the way we look at the disease and potentially make the statistics a lot less dire.
Unlike some of the promising treatments that have failed in 2017 that deal with the so-called “amyloid hypothesis” (the treatments target amyloid beta deposits in the brain that accumulate in people with Alzheimer’s disease), approaches that try to prevent nerve cells from dying wouldn’t have any impact on that buildup. Instead of trying to clear the body of the deposits, it would just try to strengthen the nerve cells that are there.
“What we’re trying to do is make your nerve cells more resistant to damage,” Ray said. “It won’t stop the damage, but it’d just make them more resistant longer, be more resilient.
Researchers in Georgia have used laser-heated gold nanorods to disable the mechanism cancer cells use to spread to other sites in the body (a process called metastasis) — which is “the primary cause of cancer-related deaths,” the researchers wrote in the study recently published in PNAS.
Precisely, the method works by attacking the lamellipodia and filopodia — aspects of the cell’s cytoskeleton that act like legs, allowing it to migrate. When cells turn cancerous, production of lamellipodia and filopodia can go into overdrive.
The gold rods inhibited this transportation mechanism in two ways. First, the rods were armed with molecules that attracted and trapped the cellular machinery that caused the overproduction of lamellipodia and filopodia. Second, the rods were heated with a low energy laser of infrared light. Moustafa Ali, first author on the study, said in an interview for a Georgia Tech press release, “the light was not absorbed by the cells, but the gold nanorods absorbed it, and as a result, they heated up and partially melted cancer cells they are connected with, mangling lamellipodia and filopodia.”
A Possible End to Cancer?
The new method has not been tested in humans yet, so many more studies must be done. But, if shown to be effective, it has the potential to help millions. The American cancer society predicts that, in 2017 alone, 1,688,780 new cancer cases will be diagnosed, and 600,920 people will die from the disease.
The gold nanorods the the most potential to help head, neck, breast, and skin cancer sufferers in particular, as the ideal depth for the laser to heat the nanorod is two to three centimeters (about an inch) beneath the skin’s surface. It is an especially attractive option promising because it is less invasive than current treatments.
It would also not harm healthy cells, making it a preferable treatment to chemotherapy, which often kills cells without discrimination. It would have reduced risk for toxic side effects, and — due to its mildness — could likely be used repeatedly.
This is one of many promising cancer treatments on the horizon that could mark the end of the prevalence of the second biggest killer in the U.S. Recently, the FDA has fast-tracked testing of Pembrolizumab (branded Keytruda), which significantly shrunk and stabilized tumors in 66 of 86 test patients. A new test, backed by Bill Gates and Jeff Bezos, has been discovered that has significant potential in diagnosing cancer. These all could be tools for extending human lifespan and reducing suffering in our world.
Cancer patients are all too familiar with the debilitating effects of chemotherapy, still a mainstay of treatment for many malignancies. But as some researchers work to find new drugs, others are working to create new drug-delivery tools. Some of that work involves hacking things like virus particles and bee venom— even sperm cells.
The goal of the research is to find ways to target the delivery of cancer drugs more effectively in order to boost their effectiveness and alleviate side effects— which in some cases are no less dangerous than the cancer itself.
“Some chemotherapy drugs can destroy patients’ hearts or kidneys,” says Daniel Kohane, a Harvard Medical School professor whose lab conducts research on biomaterials and drug delivery.
Chemotherapy works essentially by killing fast-growing cells. But cancer cells aren’t the only ones in the body that reproduce rapidly. Cells in the intestinal lining turn over quickly. Ditto for hair follicles and blood cells. So as chemo takes on cancer cells, it’s also damaging healthy cells.
“Only about 0.1 percent of the drug molecules actually reach and go into the tumors,” says Haifa Shen, an associate professor of nanomedicine at the Houston Methodist Research Institute who studies drug delivery methods. “Over 99.9 percent of chemo drug molecules stay outside of the tumors, being very toxic to normal tissues.”
Viruses vs. Breast Cancer
Viruses are promising drug-delivery tools because, once inside the body, they’re great at finding their way to specific types of cells while avoiding other types. Cold viruses target cells lining the nose, throat, and lungs, for example, while the Ebola virus attacks cells in the liver and arteries. Once inside their target cells, viruses unload their cargo of genetic material and set the stage for the production of more virus particles.
It would be a major advance in cancer therapy if researchers could find a way to modify viruses so as to retain their targeting capabilities while swapping out their genetic cargo for potent anticancer molecules. And Frank Sainsbury and his team at the University of Queensland in Australia are doing just that. In a series of preliminary experiments, the scientists created “fake” viruses whose outer shells, or capsids, were engineered to attach only to breast cancer cells.
“It’s somewhat similar to how two magnets interact with each other, and we can build the capsid’s surface that way,” Sainsbury says.
Sainsbury started off with Bluetongue, a virus that affects only cows and sheep. Using tobacco plants as incubators, the team created empty Bluetongue capsids and then loosed them on breast cancer cells in a petri dish. The shells did what the scientists hoped they would. They found their targets, and the cancer cells “took them in,” according to Sainsbury.
Bluetongue shells make good drug delivery vehicles because they can carry a lot. “They are big shells with a lot of cargo space that we can fill with drug molecules,” Sainsbury says. He added that the next step for his research will be to load the shells with chemo drugs and get them to unload their cargo to kill tumors.
Modified Bee Venom
Cancers vary in lethality, and brain cancer is often a death sentence— in part because few drugs are able to reach the brain.
The brain is separated from the rest of the body by a protective membrane that keeps out microbes, viruses, and other potentially harmful organisms and substances. “Your brain is like a medieval city surrounded by stonewalls with the guards at the gates that select who can go through,” says Ernest Giralt, a professor of organic chemistry at the University of Barcelona in Spain. “So very few chemicals can get into the brain.”
Luckily, some substances are able to sneak in. One is bee venom, or apamin, which bees release when they sting.
In its original form, apamin can’t be used therapeutically because it harms nerve cells. So Giralt’s team chemically modified apamin to take away the molecule’s toxic effects. The team injected mice with the modified apamin and observed no side effects. And the modified apamin crossed the brain membrane even more easily than the original version. “It was pure serendipity,” Giralt says.
The team is now exploring the best way to use apamin to shuttle chemo drugs into the brain. There seem to be two ways to do it, Giralt says. One would be simply to attach a chemo molecule to modified apamin. The other would be to fashion a sort of “bulk shipment”— basically stashing a load of chemo into a virus shell studded with apamin molecules and testing whether it can pass through the membrane.
‘Spermbots’ to the Rescue
Hardly anyone would think of sperm as a tool to fight cancer, but a group of researchers at IFW Dresden and Chemnitz University of Technology in Germany did. Their preliminary research suggests that it might be possible to turn sperm into “sperm-hybrid micromotors” able to deliver chemotherapy agents to malignancies of the cervix, ovaries, or uterus.
Sperm, of course, have evolved to navigate the female reproductive tract. They neither damage tissue nor cause toxic side effects. To create the spermbots, the scientists soaked bull sperm cells in the cancer drug doxorubicin and then “dressed” the cells with tiny iron-coated mesh. Then they used magnets to steer the cells toward tumor cells in a petri dish.
Three days later, only 13 percent of tumor cells were still alive–a level of effectiveness far superior to that seen when doxorubicin was delivered without spermbots.
The scientists foresee a day in which patients with gynecological cancers might lie inside a magnetic chamber where an electromagnetic field would direct the sperm cells to their target. “It would be somewhat similar to lying inside an MRI machine,” says Haifeng Xu, lead author of a paper describing the research.
NBC Universal Media, LLC on June 26, 2017 by Lina Zoldovich. Copyright 2017 NBC Universal Media, LLC. All rights reserved.
A new report from the Canadian Cancer Society (CCS) predicts that almost 50 percent of Canadians will be diagnosed with cancer, and half of these (25 percent of Canadians overall) will die from the disease. This makes cancer the leading cause of death in the country. The diagnosis rate for men is 49 percent, while for women it is 45 percent.
More than half of these cases are accounted for by prostate, breast, colorectal, and lung cancers. Lung cancer specifically was noted to kill more than the other three combined, and 85 percent of its cases were caused by smoking. However, pancreatic cancer is the most deadly form in terms of percentage of people killed post-prognosis, with 5,500 Canadians to be diagnosed and 4,800 of these dying.
The CCS stated that “the rise in cancer cases is primarily being driven by an aging and growing population. According to today’s report, an estimated 206,200 Canadians will be diagnosed with cancer this year, and almost 90 percent of these cases will be among Canadians 50 years of age and older.” While this news is shocking, it has not bucked the upward trajectory of cancer treatment in Canada: the five-year cancer death rate has decreased from 75 percent in the 1940s to 40 percent today.
Changing lifestyle choices is the key to decreasing your likelihood of cancer, said Leah Smith, CCS epidemiologist and one of the report’s authors. She said in an interview for a CCS press release, “Actions like quitting smoking, eating well, being physically active and practicing sun safety, along with appropriate cancer screening tests, can go a long way to reducing your risk of getting cancer.”
What We Can Learn
The research was a collaborative effort between the CCS, the Public Health Agency of Canada, Statistics Canada, and provincial and territorial cancer registries. This collaboration is crucial because it gives an objective viewpoint and provides new statistics that, according to the CCS, “are a better reflection of the risk of being diagnosed with cancer at some point in life.” Without cooperation between different branches of the civil sector, such objectivity would be impossible.
The news, while tragic, serves to highlight the benefits of open information because Canadians — along with the rest of the world — can make changes to their lifestyles to lower their risk of adding to these cancer cases. It may also encourage more individuals to make appointments with doctors for possible cancer symptoms, which is vital, as early detection is one of the most powerful weapons against cancer.
There are promising pieces of research worldwide that focus on cancer detection and treatment — although there could be more of these as the CCS claim that 60 percent of high-priority research goes unfunded. Pivotal work includes a new blood test, backed by Bill Gates, that can detect cancer; a possible new cancer treating drug called Pembrolizumab that has been fast-tracked by the FDA for its potential; and the development of a cancer vaccine that could inhibit cancer development in the first place.
Treating cancer can be tricky: for one, cancer cells tend to spread quickly, known as metastasis — a behavior which sometimes goes undetected. As such, cancer remains a global problem, causing nearly 1 in every 6 deaths worldwide, according to the World Health Organization. 90 percent of those deaths occur when the cancer has metastasized. But what if the spread of cancer cells could be prevented? That’s the idea behind a study a team of researchers from Johns Hopkins University published in a recent issue of the journal Nature Communications.
The researchers realized the key is understanding what triggers metastatic behavior. “We found that it was not the overall size of a primary tumor that caused cancer cells to spread, but how tightly those cells are jammed together when they break away from the tumor,” lead author Hasini Jayatilaka said in a press release. The same kind of cellular behavior is also found in bacteria.
“At a fundamental level, we found that cell density is very important in triggering metastasis. It’s like waiting for a table in a severely overcrowded restaurant and then getting a message that says you need to take your appetite elsewhere.”
Improving Patient Outcomes
Prior to this study, the common notion about metastasis was that it occurred as a result of tumor growth. The team studied tumor cells in a three-dimensional environment mimicking human tissue and found that crowded conditions in cancer cells — not necessarily the tumor’s growth — is what triggers metastasis. They also identified the proteins — Interleukin 6 (IL-6) and Interleukin 8 (IL-8) — that cause cancer cells to spread.
“By doing this, we were able to develop a unique therapeutic that directly targets metastasis, not the growth of the primary tumor,” senior author Denis Wirtz explained in the press release. “This treatment has the potential to inhibit metastasis and thus improve cancer patient outcomes.”
Boston University professor Muhammad Zaman found this to be what’s so “exciting” about the findings of this study. “This paper gives you a very specific target to design drugs against,” he told the Baltimore Sun. “That’s really quite spectacular from the point of view of drug design and creating therapies.” The researchers note, however, that one drug or one therapy alone won’t do the trick. It’ll take drug cocktails, or a combination of various treatments that target metastatic behavior together with the body’s immune system, to win the battle against cancer once and for all.
One new drug has doctors and pharmaceutical companies in a tizzy. Pembrolizumab (branded Keytruda) has recently been approved, in a hurry, by the Food and Drug Administration (FDA) to treat multiple tumors that arise from cancer in individuals with the same genetic abnormality.
During a clinical trail, the drug was tested in 86 patients. Of those who took part in the study, 66 patients had their tumors both significantly shrink and stabilize — meaning the tumors did not start to grow again. In 18 of these 66 patients — which is 21 percent of all patients — the tumors actually completely disappeared and not grown back whatsoever.
Now, this drug wouldn’t work for patients suffering from any type of cancer. For now, it is only approved to treat patients battling select varieties of advanced lung, melanoma, and bladder tumors.
Pros and Cons
While this is exciting progress, the treatment doesn’t come cheap. Just to test whether or not you might be a genetic match for the specific mutations that the drug targets costs between $300 and $600. The treatment itself currently costs $156,000 per year.
However, there is great hope that the drug itself and others that will follow in its footsteps will eventually come down in price, because this drug is truly the first of its kind. So what makes this drug so special? Well, it is the first approved drug in history that targets tumors from a specific, shared genetic profile, regardless of where the tumor is located.
Targeting tumors based off of genetic traits could help researchers and clinicians to more accurately target and treat cancers. Instead of just targeting the physical location of the tumor, treatments could be further tailored to the unique genetic profile of the individual patient. While this specific drug would only be effective for about four percent of cancer patients (though this would still help tens of thousands of patients), it could lead to a future where tumors are better targeted with genetic testing.
New research from scientists at the University of Nevada, Las Vegas (UNLV) shows that the cancer risk for astronauts undertaking long-term missions to Mars or any other destination beyond Earth’s magnetic field is actually twice what we previously thought.
In the past, researchers determined that exposure to the very high rates of ionization in the atoms that comprise cosmic rays damaged the cells in astronauts’ bodies, making them vulnerable to a range of health problems, including acute radiation syndromes, cancer, cataracts, central nervous system issues, and circulatory diseases.
The actual amount of risk has typically been assessed using conventional risk models that attributed the radiation cancer to DNA mutation and damage, and these previous studies involved much briefer periods of time than those that occur during long-term space missions.
The researchers in the UNLV study used a non-targeted effect model instead. This model, which shows higher cancer risk in bystander cells in close proximity to heavily damaged cells, reveals a cancer risk at least twice that of the conventional risk model.
“Galactic cosmic ray exposure can devastate a cell’s nucleus and cause mutations that can result in cancers,” UNLV researcher and space and radiation physics scholar Francis Cucinotta explained in a press release. “We learned the damaged cells send signals to the surrounding, unaffected cells and likely modify the tissues’ microenvironments. Those signals seem to inspire the healthy cells to mutate, thereby causing additional tumors or cancers.”
Combatting Cosmic Radiation
Any extensive time outside the Earth’s geomagnetic sphere will produce this much higher level of risk, and Cucinotta asserts an urgent need for additional research on human cancer risks and cosmic ray exposures prior to any long-term space missions. The results of this study will clearly affect the predicted efficacy of any already planned responses, such as radiation shields, so those must be reassessed, as well.
“Exploring Mars will require missions of 900 days or longer and includes more than one year in deep space where exposures to all energies of galactic cosmic ray heavy ions are unavoidable,” Cucinotta stated in the release.“Current levels of radiation shielding would, at best, modestly decrease the exposure risks.”
Cucinotta also addressed the moral dilemma we now face as we strive to colonize Mars and travel in space: “Waiving or increasing acceptable risk levels raises serious ethical flags, if the true nature of the risks are not sufficiently understood.” Indeed, we owe it to the astronauts willing to risk their lives to explore space to do everything we can to make sure they return home as healthy as when they left.
Specifically, the research involved using phytocannabinoids — the naturally-occurring cannabinoids in the cannabis plant — in tandem with chemotherapy. “Phytocannabinoids possess anticancer activity when used alone, and a number have also been shown to combine favorably with each other in vitro in leukaemia cells to generate improved activity,” according to a study published in the International Journal of Oncology.
Though the tests were done in the laboratory, the researchers are confident that combining phytocannabinoids with chemotherapy for leukemia patients could mean lower doses for the latter — effectively lessening its side-effects.
In Concentrated Doses
As with most studies involving cannabis, it’s worth mentioning that it’s not possible to achieve the effects claimed by the study by recreational use of the drug. “These extracts are highly concentrated and purified, so smoking marijuana will not have a similar effect,” lead researcher Wai Liu said in a press release. “But cannabinoids are a very exciting prospect in oncology, and studies such as ours serve to establish the best ways that they should be used to maximize a therapeutic effect.”
Cancer research is one of the busiest fields in medical technology, and understandably so, as cancer remains one of the leading causes of death worldwide. While there are existing treatments available for cancer, these usually cause a terrible amount of strain on the body and aren’t always effective. But what if much of that could be avoided by early detection using a simple, non-invasive test? Researchers from the Memorial Sloan Kettering Cancer Center and genomics company Grail are close to developing such a procedure.
According to a study published in the Journal of Clinical Oncologyand presented on Saturday at the annual meeting of the American Society of Clinical Oncology (ASCO), a technology to test for cancer years before its symptoms manifest just delivered promising results in an early-stage feasibility study. This technology, referred to as liquid biopsy, scans the blood for traces of DNA shed by tumors — or circulating tumor DNA.
“Our findings show that high-intensity circulating tumor DNA sequencing is possible and may provide invaluable information for clinical decision-making, potentially without any need for tumor tissue samples,” lead researcher Pedram Razavi told Medical Xpress.
For the test, however, the researchers had to rely on samples of 124 metastatic lung, breast, and advanced prostate cancer cells taken from blood and tissues of patients. Scanning for 508 different gene mutations, they detected 864 genetic changes in the tissue samples and 73 percent of these were found in the blood as well.
At least one mutation was spotted in both the cancer tissue and blood samples in 89 percent of the patients, with breast cancer detection succeeding 97 percent of the time.
“Our combined analysis of cell-free DNA and white blood cell DNA allows for identification of tumor DNA with much higher sensitivity, and deep sequencing also helps us find those rare tumor DNA fragments,” Razavi explained in the interview with Medical Xpress.
Researchers from the University of Southampton and the University of Edinburgh have found that it’s possible that the more coffee you drink, the less likely you are to develop hepatocellular cancer (HCC) — the most prolific form of liver cancer. Analyzing data from 26 studies, which involved more than 2.25 million participants in total, they concluded that people who drink 1 cup of coffee per day have a 20% reduced risk, 2 cups per day reduces risk by 35%, and 3 cups per day decreased risk by 50%. These findings showed that decaffeinated coffee also affects your risk, but the team could not deduce the precise amount.
Lead author Dr. Oliver Kennedy, a member of the Primary Care and Population Sciences Faculty of Medicine at the University of Southampton, told The Guardian: “Coffee is widely believed to possess a range of health benefits, and these latest findings suggest it could have a significant effect on liver cancer risk.” Coffee has also been said to have painkilling capabilities and the potential to prevent heart attacks.
Decaf Drinkers Win Too
The main consequence of this study is that doctors may be able to use coffee to help in the prevention of liver cancer. It’s a step that is both inexpensive and easy for people to incorporate into their daily lives, if they haven’t already. These benefits are also present in decaffeinated coffee, meaning that this means of prevention would also be accessible to those who can’t or do not drink caffeinated coffee.
The study authors wrote “It may be important for developing coffee as a lifestyle intervention in chronic liver disease, as decaffeinated coffee might be more acceptable to those who do not drink coffee or who limit their coffee consumption because of caffeine-related symptoms.”
Now, this development is not necessarily an encouragement to drown yourself in Starbucks. There are dangers in consuming too much caffeine, and much more research still needs to be done before coffee can be used medically with certainty. There is not enough existing research into the possible repercussions of consuming large quantities of caffeine over time, especially as a preventative medical measure. Hopefully in the future, preventing liver cancer will be cheap, easy, and delicious.
Nanomaterials are engineered devices so small that they can only be measured on a molecular scale. These microscopic machines come in many shapes and can be made out of many different kinds of material, from gold to synthetic polymers, depending on their designed functions — which are numerous and varied.
The benefits of using nanomaterials in medicine are many, especially when it comes to cancer therapies. Right now, these machines are being used to selectively deliver toxic chemotherapy to cancer tumors, reducing the doses required to kill the tumors and the risks of serious side effects for the patient. In the future, nanotherapeutics may be engineered to kill cancer cells themselves, possibly activated near-infrared light.
These life-saving technologies have sparked a surge of research that has grown since the early 2000s. And while many researchers have been eager to test their nanomaterials for anti-cancer activity, they have had few tools for doing so.
A Novel Platform
To put this in perspective, let’s take a look at the pharmaceutical industry. Conventional drug developers have streamlined their process of drug discovery and development, but even so, 90 percent of potential drugs that pass all of their cellular and animal tests fail in clinical trials when tested in humans. This represents billions of dollars wasted that might have been spent on drugs that could actually help people. And this is the reality for an industry that already has a myriad of tools for testing their drug candidates. Just imagine the hurdles faced by an entirely new class of therapeutics that has precious few of these tools. Such is — or was — the case for nanomaterials.
“This is an important step forward for the field,” principal investigator, Alexander Stegh, said in an interview for a Northwestern press release. “The very thorough optimization that we see in conventional drug development had been missing in the nanotech space, and we felt very strongly about changing this. The system that we developed here really allows us to support those efforts.”
Stegh’s team used the platform to test the therapeutic nanomaterials they were developing — spherical nucleic acids (SNAs), which may be able to kill a currently incurable type of brain cancer by targeting a particular gene. Their system allowed them to see that the nanoparticles had the greatest effect between 24 and 48 hours after administration, giving them an idea for the best time frame to administer additional chemotherapy.
While this study demonstrates some potential for SNAs to one day help patients with brain cancer, the platform itself may have the greatest impact on our treatment options, said researcher Timothy Sita.
“It’s a platform to help optimize the drugs in mice before they go to human trials and make something that will translate better to the clinic,” Sita said in the press release. “Now we can tweak these particles — play with the shape of the nanoparticle, or how much RNA we load onto the particle, for example — and then assess very quickly whether those changes are more effective or not.”
Cancer is terrifying since the disease manifests within a person’s own malfunctioning cells. From the moment when the cell cycle goes amuck and cells begin to divide aberrantly with no end, every second counts. That’s why one vital factor in tackling cancer is early detection. Patients whose cancer is detected sooner often have an increased chance at recovery. This is especially true with lung cancer patients, whose chances of survival increases by 200 percent when cancer is detected early.
The technique seems pretty simple in that scientists collect DNA fragments from dying cells in your blood. In theory, a patient with cancer in the earliest stages should have some population of dying cancer cells that shed fragments into the bloodstream. A quick, affordable, and noninvasive blood test can analyze the blood for any cancerous DNA.
The test is so good that it can determine that cancer is growing before tumors are even detectable on traditional CT scans and far before patients first feel symptoms. The new technique was tested in a trial with 100 lung cancer patients who were followed from diagnosis through surgery and chemotherapy.
Results following the trial of the Liquid Biopsy technique are published in Nature. Patients who had residual amounts of tumourous DNA detected in their blood would go on to relapse in months or even a year after their cancer was removed. With the technique, doctors were able to predict a relapse in a patient within a 350-day window with a startling 92 percent accuracy.
This technique shows real promise in diagnosing cancer early at an affordable cost. Once the system is thoroughly developed, scientists like Lo suggest that routine blood tests may provide the ultimate cancer screen. Advances like the Liquid Biopsy display the power that lies in personalized medicine, a health care strategy aiming to provide each patient with care customized to their body.
One form, esophageal cancer, is diagnosed in 16,940 people each year. This type has a five-year-survival rate of only 18 percent. A major reason for this is timeliness of diagnosis: esophageal cancer is difficult to detect, and screening methods are quite invasive — ranging from esophagoscopy, biopsy, balloon cytology, chromoendoscopy, and fluorescence spectroscopy.
Even if screenings are done in a timely manner, the tests do come with their own risks and side effects, and can sometimes detect false positives — or even false negatives. With more intense methods like esophagoscopy and biopsy, there are serious side effects including a puncture of the esophagus, trouble breathing, the passage of food in the airway, or even an increase in heart attack risk.
Down The Hatch
That being said, the challenge for researchers and clinicians has long been devising less invasive tests that are lower risk and ideally, cost efficient, too. Researchers at the University of Cambridge have developed something known as the Cytosponge to detect Barrett’s esophagus, a condition that increases one’s chance of developing esophageal cancer.
Unlike more traditionally invasive tests, the Cytopsponge has a patient swallow a capsule attached to a string. The capsule contains the sponge, which then expands in the stomach when the capsule is dissolved. A nurse then pulls the sponge out, allowing the surface of the sponge to collect cells from the esophageal lining on its way up, which can be then be tested.
The new screening method is still undergoing clinical trials. Presently, the research team is searching for 9,000 patients over the age of 50 who are on long-term acid-suppressant medication. This is the final step before the promising innovation could be adopted in mainstream practice.
Testing with the Cytosponge takes just five minutes, and is far more affordable for patients to undergo than a traditional endoscopy screening. Using the Cytosponge as a regular test for esophageal cancer, could potentially increase the early detection of malignancies and, hopefully, save more lives.
Aspirin has long been considered something of a wonder drug, able to do everything from treat headaches to stave off heart attacks. Now, scientists believe it may also be able to prevent cancer cells from spreading after a tumor has already formed in the body.
For a tumor to spread, its cells must travel through the bloodstream to a new location where they then settle and grow, all without being detected by the immune system. Helping them during this process are cells called platelets. These cells do everything from cloak the cancer cells during their trip to help them receive nutrients and oxygen once they reach their new location.
In tests with mice, Elisabeth Battinelli, a hematologist at Brigham and Women’s Hospital in Boston, found that aspirin actually prevented platelets from assisting malignant cells on their journey to a new home, thus making it more difficult for the cancer to spread.
Not for Everybody
Each year, 1.6 million people are diagnosed with cancer in the U.S. alone, and nearly 600,000 die as a result of their disease. Unfortunately, aspirin won’t be able to help all of those people – in fact, it could actually worsen the health of some by causing side effects like bleeding.
Right now, knowing who will benefit from aspirin and who won’t is something of a crapshoot.
“It’s challenging to develop a single molecular test that will tell you if someone will respond [to aspirin] or not because it’s become clear that there is no single pathway by which aspirin works,” Andrew Chan, an epidemiologist at Harvard Medical School, told Scientific American.
Researchers are already looking into the genes involved in aspirin’s affect on platelets, and they hope to develop a genetic test to tell whether aspirin would be an effective treatment for an individual. Until then, studies of larger, more varied groups of people should provide insight into the cancer-fighting prowess of this common yet extraordinary medication.
Cancer is when an aberrant mutation in a cell leads it to prolifically divide, causing abnormal cell growth that can potentially spread to other parts of the body if untreated. Cancer is the second leading cause of death globally, with one in every six deaths caused by a type of cancer in 2015, leading to 8.8 million deaths.
Because different mutations can cause cancer, and cancerous cells can develop in many different parts of the body, doctors are continually coming up with different strategies for treating the disease. With each passing year, research on the topic continues to progress. From personalized vaccines to mecha-suit sperm, we’ve been looking in every possible nook and cranny in hopes of finding an effective therapy that can work better than what we have today.
Currently, we use a host of methods to treat cancer, including surgery, radiation therapy, chemotherapy, immunotherapy, targeted therapy, hormone therapy, stem cell transplant, and precision medicine. While some cancer patients receive only one treatment, these treatments are normally used in conjunction to increase the rate of success.
Since the 1960s, our efforts in tackling cancer have progressed significantly. Patients back in the day had a five-year survival rate of around 50 percent. With the advent of these new therapies, some the most commonly diagnosed cancers in the U.S. have 5-year-survival rates at around 75 percent.
The next step in cancer therapies might be quietly waiting for its time in the limelight in Seattle, Washington, at the Fred Hutchinson Cancer Research Center, where scientists have constructed biodegradable nanoparticles that can genetically program immune cells while inside the body to target cancer cells. The study was published on April 17 in Nature Nanotechnology and focused on the effect that nanoparticle-programmed immune T cells had on leukemia in mouse models.
The nanoparticles carried genes that code for chimeric antigen receptors (CARs), which are proteins designed by scientists to help immune cells target and destroy cancer. Once the immune cells undergo this molecular modification, they turn into an army of cancer serial killers.
This new method can eliminate expensive and time-consuming steps that lag previous T cell cancer therapies. The current protocol is that the T cells are removed from the patient, genetically altered, regrown, and infused back into the patient. The biodegradable nanoparticles will eliminate the removal, regrowth, and infusion steps by accomplishing the reprogramming step over a time span of 24 to 48 hours while the T cells are in the body.
When the researchers compared the nanoparticle-based method to current immunotherapy methods that require the T cells to be removed, researchers noticed that leukemia-induced mice lived an additional 58 days on average when compared to the mice that received the current treatment.
While these results are exciting, the researchers are looking to make the process safer before they move into human trials. But if this new technique is approved for humans, it could have many more applications. Scientists are looking to adapt the method for diseases like hepatitis, HIV, or even solid tumors.
By quickly arming patients’ immune cells to fed off disease, this new treatment could lower healthcare costs and improve the quality of patients’ lives.
Cancer comes in many different forms, and it is not unusual for diagnosed patients to endure multiple kinds of treatments before one that is effective against their particular form of cancer is found. If it takes too long for doctors to find the right treatment, the consequences can be fatal.
While earlier cancer vaccines targeted a singular cancer protein found ubiquitously among patients, these personalized vaccines contain neoantigens, which are mutated proteins specific to an individual patient’s tumor. These neoantigens are identified once a patient’s tumor is genomically sequenced, providing physicians with the information they need to pinpoint unique mutations. Once a patient’s immune system is provided a dose of the tumor neoantigens, it can activate the patient’s T cells to attack cancer cells.
Neoantigens To The Rescue
Unlike previous attempts towards cancer vaccines, which did not produce conclusive evidence in halting cancer growth, Wu’s team made their personal vaccine much more specific to each patient’s cancer, targeting about 20 neoantigens per patient. The vaccines were injected under the patients’ skin for a period of five months and indicated no side effects and a strong T cell response.
All of Wu’s patients who were administered the personal vaccine are still cancer-free more than 2.5 years after the trial. However, some patients with an advanced forms of cancer also needed an some extra punching power to fend off their diseases. Two of Wu’s patients who did relapse were administered an immunotherapy drug, PD-1 checkpoint inhibitor, in addition to the personalized vaccine. Working in conjunction with the enhanced T cell response from the vaccine, the drug makes it difficult for the tumor to evade the immune cells. The fusion of the two therapies eliminated the new tumors from both patients.
But we can’t get too excited yet. While these results are promising, the therapies are relatively new and require much more clinical testing. Many physicians around the world are working together to test the potency of neoantigens in order to verify if the vaccine works better than current immunotherapy drugs over a sustainable period of time. Personalized vaccines are costly and take months to create, a limiting factor in providing care to patients with progressing cancers.
Still, this study is an encouraging sign for many oncologists who are interested in using the immune system to fight cancer. More than a million new patients are diagnosed with cancer each year in the U.S. alone, and even in situations where the cancer is treatable, the available chemotherapy agents themselves can be very toxic. If proven safe and effective, this personalized cancer vaccine could give patients around the world hope for powerful treatment with fewer side effects.
Humanity’s battle with cancer has goaded us to turn to some of the most unconventional therapies possible in hope of combating the deeply emotional and turbulent disease. Physicians are prescribing electric caps like the Optune to zap tumors away, while others are suggesting the analysis of a quick breath can detect cancer. There might be something a little bit more unorthodox on the horizon to tackle cancer: physician scientists from the Institute of Nanosciences in Germany claim the answer may be human sperm.
Mariana Medina-Sánchez and her team led a study looking into the unique drug delivery benefits human sperm could provide. The team noticed that when sperm are submerged in an active ingredient found in cancer treating drugs, it can absorb large doses. The sperm can then be assembled into microscopic mechanical harnesses, creating sperm-hybrid micromotors. The iron in these harnesses allows clinicians to manipulate the direction of the sperm with external magnetic fields, which in turn allows doctors to direct the drug-coated sperm in the direction of the tumor.
Once the metal harness reaches a surface, its quick release system relinquishes its grip on the sperm’s and allows them swim away once they reach their target. In theory, this would enable the sperm to burrow deeper into tumor tissue, exposing more cancer cells to the drugs in a more direct way than has been possible by other current treatments.
While Medina-Sánchez’s team has only experimented with bull sperm (as they are similar in size to human sperm) the team noticed that the sperm-hybrid micromotor reduced cancerous cells by 87% in just 72 hours. The method proved to be far more effective than treating cancer cells with the drugs alone.
Revolutionizing Drug Delivery
The sperm-hybrids could be potentially advantageous for the hundreds of thousands of women with gynecological cancers, and perhaps even other diseases of the female reproductive tract. The sperm-hybrid micromotor boasts significant advantages: not only do sperm cells provide added protection when it comes to keeping the drug from degrading prematurely. They also wouldn’t unnecessarily trigger the immune system, like a drug piggybacking on bacteria would.
Drug delivery comes in many forms: swallowing, inhalation, absorption through the skin, or intravenous injections. That being said, it’s not surprising that nanotechnology is a hot topic in drug delivery. Even with new technologies, science seems to have stagnated around several central topics: delivering drugs past the blood-brain barrier, enhancing individual cellular delivery, and combining diagnostics and treatments.
Chemotherapies that inadvertently target non-cancerous cells result in the death of normal cells. This is a consequence that can be avoided if Medina-Sánchez’s sperm-hybrid micromotors are approved by national standards.
While Medina-Sánchez’s new approach does have many questions to left to answer — including how sperm could be introduced into the reproductive system as drug-delivery agents while not also potentially causing pregnancy — the method certainly seems promising.
Many artificial organs are being developed as an alternative to donated organs, which are only temporary solutions that require the recipients to maintain a lifetime regiment of medications. With recent advancements in biomedical technologies, the time may be coming when those who require transplants no longer need to wait on donation lists to replace organs like kidneys and blood vessels. And now, scientists have added the thymus to the list of body parts we can artificially simulate.
The thymus is a gland that is essential to your immune system. T cells, a type of white blood cell that helps to get rid of viruses, bacterial infections, and cancer cells, mature within this gland. When people get sick (or as they age), the thymus becomes worse at its job. In some cases, people with different types of cancer are not getting the biological support and help they need from their T cells.
Now, there are adoptive T cell immunotherapy treatments which involve removing T cells from a patient, “fixing” them, and transfusing them back. But these treatments depend on the patient actually having enough of these cells, and many do not. This type of treatment also takes a very long time to complete.
To create a more sustainable and effective solution to this serious medical issue, researchers at UCLA created artificial thymic organoids that create T cells from blood stem cells. This was an incredible feat in medical science — but could these artificial structures create specialized T cells that have cancer-fighting receptors? Yes.
The team inserted a Gene for cancer-fighting receptors into blood stem cells. This caused the organoids to produce only cancer-specific T cells. Because other types of T cells could accidentally target and attack healthy tissue, these results are exceptionally positive. If specific T cells can be created and other types turned off, cancer cells can be targeted and attacked without causing autoimmunity problems.
The researchers published their work in Nature Methods and are now investigating this technique with pluripotent stem cells. This could allow for the creation of a more sustainable supply of these life-saving cells. The team is calling on other scientists to reproduce its work.
This new development could be one large step towards reducing the costs of cancer treatments. It is no secret that most modern cancer treatments are either extremely costly, dangerous to healthy tissues, not effective enough, or a combination of these. There are many treatments that successfully put patients into remission and allow them to continue on with healthy and fulfilled lives. But, there is still a lot of room for improvement, and this could be one of them.
Although this patented artificial structure will have to go through years of clinical trials before it can be widely adapted by the medical community, and it has not been tested in humans yet, it holds promise as a way to guarantee the creation of healthy cancer-targeted T cells. The availability of treatment may not depend on a patient’s existing cells that must be removed and engineered. Instead, patients of varying levels of illness could have equal access to treatment — and to hope.
Cancer, the emperor of all maladies, is tragic under most any circumstances, but it’s even worse when the condition could have been prevented. Scientists estimate that 40 percent of all cancers are preventable, and those figures include several types you may think of right away, such as lung cancer (the most deadly) and skin cancer (the most preventable). Thanks to improved diagnostics and surveillance technologies, early cancer detection is one benefit of living in the 21st century. But how do we go about preventing the 40 percent of cancers that are preventable?
According to the WHO, a third risk factor is alcohol, which is estimated to be responsible for more than 300,00 cancer deaths yearly. The substance can cause cancer of the mouth, liver, breast, or colon. However, the risk of cancer is dependent on how much alcohol is consumed, so moderate amounts shouldn’t be the source of too much worry.
So that’s 40 percent of cancers, but what about the other 60 percent?
In the award-winning television series “Breaking Bad,” the general conflict arises when a high school chemistry teacher is unexpectedly diagnosed with lung cancer. With no history as a smoker, his bad luck pushes his already struggling family into further debt to pay his medical bills, which leads to an interestingplot. Unfortunately, the brooding anti-hero’s surprising cancer diagnosis might be more common than we thought.
Mutations occur each time our cells divide. Usually, these mutations take place in segments of DNA that aren’t very important. However, if a mutation occurs in a cancer driver gene, we might suffer from some bad luck. In their paper, Vogelstein and Tomasetti report that 66 percent of mutations are random, 29 percent are caused by environmental factors, and 5 percent are due to hereditary factors.
The JHU team asserts that these mutations aren’t the be-all-end-all of cancer — they’re just one factor in the process of its development. To that end, other scientists suggest that we must study the interplay of other factors, such as hormones, with genetic mutations to get a better understanding of the whole picture.
While learning that the majority of cancers appear to be unavoidable isn’t the most heartwarming news, it does leave us with the knowledge that the other 40 percent are preventable, giving us some control over our health with respect to this awful disease.
Imagine this: you’re a physician at one of the most renowned medical institutions in the world. A patient comes in with a very aggressive form of cervical cancer and you collect her cells to study them for her particular case. But while studying her cells, you notice something odd. After a certain number of cell divisions, they don’t die like other cells in the research lab. In fact, they don’tdie at all.
It’s the year 1950 and it’s years before any regulations on harvesting cells from patients are mandated. In fact, there is no custom of asking permission for cell collection for research. With that said, you think about all the potential these “immortal cells” may have. You have never seen cells quite like them before in your life, and you know for a fact that your colleagues and other researchers around the world have not either.
What do you do?
To George Otto Gey, it was simple: collect the cells and propagate them for future research. His patient was a 31-year-old woman named Henrietta Lacks.
The birth of a medical revolution
Henrietta Lacks’s cancer cells were quickly dubbed “HeLa cells” in the scientific community. Even 60 years after their collection, HeLa cells are still the most commonly-used cell line around the world, having been produced billions and billions of times now. This is because HeLa cells were the first cells to survive in vitro (in a test tube) and provided the foundation for some of the most remarkable discoveries in modern medicine.
If you have ever had the polio vaccine, you can thank Henrietta Lacks for her cells. From 1840 to 1950, Poliomyelitis was a lethal global epidemic that not even President Franklin D. Roosevelt was spared from. He declared a war on the disease. The vaccine developed by Jonas Salk in 1952 was only possible because HeLa cells were able to survive in vitro. The HeLa cells were easy to infect and study, and therefore provided the perfect subject for Dr. Salk to utilize in his research. With only 403 cases in 2014, polio has been on the run. The vaccine has prevented 650,000 deaths and 13 million cases of paralysis since 1988. All of this would not have been possible if it weren’t for Henrietta Lacks’s immortal cell line.
Henrietta Lacks’s contribution to modern medicine is clear—without her cells, who knows where we would be today? While medical progress is often thought of as inevitable, it’s by chance events like the discovery of Lacks’s cells that the rate of progress is decided. Her cells were the catalyst to many medical advances that we have today.
A high-tech cousin to the Breathalyzer may be the future of cancer detection. Trials of a simple cancer spotting breath test are underway at the University of Southern California (USC). Participants have volunteered to see if the the “BreathLink” app and it’s partner device, the Breathscanner, can detect cancer.
“It’s just like a breathalyzer for alcohol, only it’s a billion times more sensitive,” Dr. Michael Phillips of Menssana Research, who is spearheading the project, told CBS’s Susan Spencer.
Breathscanner collects human breath. Then BreathLink, a cloud application device, subjects the volatile organic compounds (VOCs) in it to concentration analysis. It uses gas chromatography to separate alveolar breath VOC samples and then detects each specific target using surface acoustic wave detection (GC-SAW) or flame ionization (GC-FID). It is sensitive to the picomolar (parts per trillion).
BreathLink has already identified patients with active pulmonary tuberculosis accurately, and these latest trials are the next step in the process. Current clinical studies include detection of lung and breast cancer, as well as heart transplant rejection. The device’s makers hope that these trials, if successful, will pave the way toward FDA approval.
Faster, Easier, Accurate Detection
A different breath test, developed at Imperial College London is based on selected ion flow-tube mass spectrometry, is also undergoing trials. Thus far, it has successfully detected esophageal and stomach cancers in 300 patients with 85 percent accuracy. Lead researcher Dr. Sheraz Markar commented to the European Cancer Congress 2017 in January:
“At present the only way to diagnose esophageal cancer or stomach cancer is with endoscopy. This method is expensive, invasive and has some risk of complications. A breath test could be used as a non-invasive, first-line test to reduce the number of unnecessary endoscopies. In the longer term this could also mean earlier diagnosis and treatment and better survival.”
Similarly, Breathscanner touts few complications, fast results, and earlier diagnosis. Since it’s a mobile point-of-care system, it can be used in the field or in an office—anywhere that has an Internet connection. It works in tandem with the BreathLink cloud application device, which uses proprietary algorithms to identify markers of disease and oxidative stress. Then, it sends data to servers in a central laboratory, where all data exchanges are protected by defense-level encryption. For patients, the process is simple: they just breathe into the device for two minutes. Less than ten minutes later, they have their answer.
When asked whether patients with cancer really have different breath, Dr, Phillips said, “The answer to that is definitely yes, for breast cancer and lung cancer.”
Dr. Markar explains why: “Because cancer cells are different to healthy ones, they produce a different mixture of chemicals.”
These two trials are signaling the future of cancer detection. Both research teams are working on detecting additional kinds of cancer in breath.
Despite the many advances in medicine over the last century, a cure for one of the most prevalent and devastating diseases in the world today continues to evade us. But thanks to new research, that could soon change.
Kite Pharma, a US pharmaceutical company, just released the groundbreaking results of their six-month gene therapy trial: terminal cancer patients in complete remission after just a single round.
The treatment filters a patient’s blood to remove T-cells, immune system cells that can be genetically engineered in a lab to identify cancer cells. Cancer cells thrive because of their ability to evade the immune system. This new therapy boosts immune cells so that they are able to eliminate cancer cells more effectively.
Patients who participated in the trial had one of three types of non-Hodgkin lymphoma. The advanced stage of their conditions meant all of them were given only a few months to live. However, following the first round of gene therapy, which took place nine months after the trial began, half the patients are not only still alive, but a third of them appear to be cured.
Among them is a 43- year-old named Dimas Padilla from Orlando, Florida whose cancer had stopped responding to chemotherapy. He completed the first round of the trial’s treatment last August, and his cancer is now in remission.
Worth The Risk?
“These results are promising and suggest that one day CAR-T cells could become a treatment option for some patients with certain types of lymphoma,” said head cancer information nurse, Martin Ledwick from the Cancer Research UK, in an interview with The Telegraph.
While the results are promising and could prove to be life- changing for patients with terminal cancer, the treatment is not without risks.
Because the therapy essentially puts the human immune system to go into overdrive by radically altering human cells, complications are certainly possible — some of which could be fatal. In fact, during the trial, two people died as a result of the therapy — not because of the cancer. Some patient’s immune systems overreacted in its effort to kill the cancer cells, while others developed blood-count related issues such as anemia. Reports of patients suffering from neurological problems were also cited, but these side effects apparently only lasted a few days.
More studies are needed to understand the therapy’s side effects, potential complications, and long-term benefits.
The trial’s full results won’t be presented until April, and the pharmaceutical company still has to get approval from the European regulatory boards — which means it will be a while yet before the therapy becomes available. Given the possible risks, it might give them enough time to study the therapy further and refine the process — hopefully eliminating any adverse effects.
Although, as the Cancer Institute’s Dr. Steven Rosenberg points out: “It’s a safe treatment, certainly a lot safer than having progressive lymphoma.”
After the doctors collected tissue using a method they dubbed stimulated Raman histology (SRH), the deep learning algorithm analyzed it. Normally during surgery, surgeons must pause the surgery for 30 to 40 minutes to allow time to process, freeze, and stain the brain tissue in a lab. Using the SRH technique and deep learning algorithm, the surgeons were able to diagnose tumors without leaving the operating room at all. Most importantly, they could cut the analysis time to just 3 to 4 minutes. This almost 90 percent decrease in diagnosing time can significantly reduce a patient’s risk for complications during surgery.
Currently, the deep learning algorithm can only identify tissues in four categories. However, Dr. Daniel Orrigner, first author of the study, aims to expand its capabilities to include eight different categories, which would cover almost all of the kinds of tumors that neurosurgeons encounter.
The Doctors of Tomorrow
Thus far, the technique has been tested on around 370 patients, with a major milestone set at 500. Right now, it has a 90 percent accuracy rate for tissue sample diagnoses. While this is less than the 90 to 95 percent accuracy rate of traditional methods, Orringer hopes he can increase the system’s accuracy over time as the deep learning algorithm will grow more accurate in its diagnoses as it has more date from which to learn.
While the current prototype is made for research purposes only, the team hopes to conduct a large-scale clinical trial to further test the program’s capabilities. They are particularly eager to bring the algorithm to small hospitals in remote parts of the country that have little or no access to neurologists. Although 1,400 U.S. hospitals perform brain tumor surgeries, only 800 board-certified neuropathologists are at work in the country. As this technology reaches more hospitals, the deep learning system can collect greater amounts of data and ensure more accurate diagnoses.
What do you get when you combine an inkjet printer, 20 minutes, a penny, and a drive to fight global health inequality?
Medical diagnostics magic.
A team of Stanford engineers have developed an alternative diagnostic method that may be a potential solution to medical diagnostic inaccessibility in developing countries. Their research, published in the Proceedings of the National Academy of Sciences, overviews a tiny, reusable microchip capable of diagnosing multiple diseases. As mentioned, the tool, which they’ve dubbed FINP, is surprisingly affordable, with a production cost of just $.01, and it can be developed in 20 minutes.
The FINP chip features three layers. The reusable top layer can be printed onto the device through a standard ink-jet printer. The bottom layer is a disposable silicon chamber that holds biological fluids, while a thin barrier separates the electronics on the top from the chamber.
These diagnostic chips are created via a simple two-step process. First, the user designs whatever custom electronic configuration is needed for a particular diagnosis. Essentially, they’re designing a circuit that will isolate molecules with distinct properties, such as a particular shape, size, density, or electronic charge, when the chip’s electronic field is manipulated. Once they have their design they can print it onto a cheap plastic sheet and place it over the single-use chambers. In the future, designs for the top layer are most likely going to be downloadable, similar to how many 3D printing designs are available today.
Diagnostics for All?
During the study, the researchers conducted tests to see if the chip could be used to pull cancer cells from a fluid sample, and it could. They also compared the efficiency of their FINP chip against a $100,000 cytometry technique typically used to count immune cells, and both tools measured the cell count accurately.
The remarkable success of testing begs the question, “How can we get this chip around the world to help those in need?” The Stanford team is working to do just that, but acknowledges that it will take some time to ensure that the device meets all standards before moving toward commercialization.
If they reach that point, they will have a device on their hands that could potentially cut costs down tremendously in diagnosing equipment while simultaneously preventing the spread of infection around the world. The team is optimistic that their device can make a difference, as they should be. A penny chip that can detect disease is one reminder that we are in the future.
Advances in medicine and technology are revolutionizing what it means to be human. By providing us with gene editing tools, such as CRISPR, we’re well on our way topersonalizing the medical revolution.
CRISPR provides a way for us to alter gene expression in particular cells, based on need. Up until recently, the process was very difficult to execute. It took many years to develop precision when altering gene expression. With the latest technology, the desired precision can be obtained in just a few weeks. CRISPR, and other technologies like it, are shaping the future of medicine.
When all possible treatments had failed, the parents of Layla, a 1-year-old with leukemia, sought help from new technology developed by Cellectis — a biopharmaceutical company based in Paris, France. The gene editing therapy, which was still experimental, had been utilized once before in a patient with HIV.
Physicians and scientists worked together to give Layla immune cells from a healthy donor that had been modified with a gene editing tool. In this case, TALEN — a DNA-cutting enzyme — was utilized to modify the donor T-cells so that they would not attack Layla’s own cells. In order for the treatment to work, a patient’s immune system is essentially destroyed and replaced with the modified cells. However, this is not a permanent fix: it’s just a temporary solution until a matching T-cell donor can be found.
While Layla’s doctors believe she is in remission, only time will tell if this was a “one-off” fix or a case that may need revisiting. Additional trials are needed so physicians and scientists can better understand how gene-editing can benefit patients, and treat diseases other than cancer.
Three years after first being diagnosed with lung cancer, Bob Berry from Manchester, UK, is now cancer-free, all thanks to his participation in a clinical trial for a mysterious new drug. The drug does not have a name, but it is reportedly used in combination with immunotherapy to help the body fight off the cancer itself.
The trial took place at The Cristie, a cancer research center that’s part of the UK’s National Health Service (NHS) and one of only six centers worldwide participating in the trial. Berry was one of the very first people to be treated with the drug a mere 12 months ago.
Prior to beginning the trial, his diagnosis was not a good one. “Three years ago, I was given 12–18 months to live, but I have already surpassed that and I feel well,” said Berry. “At the end of the day, this clinical trial has extended my life, and I couldn’t be more grateful. Anyone who is offered a clinical trial should seriously consider it.”
The Future of Cancer Treatment
According to Dr. Matthew Crebs at The Christie, “Bob has had a phenomenal response to taking part in this clinical trial. His most recent scans show that he’s had a complete response with no apparent trace of tumor in his body. We will need to monitor Bob closely with regular scans to assess how durable this response will be.”
This amazing drug could be the future of caring for cancer patients. However, it is still in its earliest trials and much more testing will be needed before the drug is available for widespread use. The doctor was also sure to mention that cancer is a very complex disease and not all patients are guaranteed to respond as remarkably as Mr. Berry. Still, this is an exciting development in the search for a cure for cancer.
An artificial intelligence (AI) algorithm, originally made to identify cats and dogs, is now diagnosing cancer.
Using an existing Google algorithm, Stanford University scientists created a dataset that they could use to train a neural network. The team gathered images from the internet and worked closely with university dermatologists and professors to collect a total of about 130,000 images of skin lesions that cover 2,000 various diseases.
Based on this database, they then taught the algorithm to differentiate between a deadly skin lesion and a patch of dry skin. The algorithm was designed to “figure out a problem rather than having the answers programmed into it,” the team said in a statement. This means that the more images it sees, the better it gets at classifying lesions.
To test the algorithm’s performance, the researchers pitted its results against the diagnosis of 21 dermatologists in three diagnostic tasks–keratinocyte carcinoma classification, melanoma classification, and melanoma classification when viewed using dermoscopy. In all three tasks, the team found that the algorithm was able to match the expertise of human dermatologists within 91 percent.
“We made a very powerful machine learning algorithm that learns from data,” said Andre Esteva, co-lead author of the paper. “Instead of writing into computer code exactly what to look for, you let the algorithm figure it out.”
AI in Healthcare
Stanford’s advanced AI may be in an early, exploratory stage at this point, but it’s not the only AI capable of delivering accurate diagnoses. Last year, doctors tapped into IBM’s AI system, Watson, to identify a type of leukemia. This AI effort helped to save a sick woman’s life. The discovery was especially remarkable given that her disease had gone undetected using traditional methods. The team at IBM stated:
The key to this success is the AI’s ability to take a massive amount of data and analyze it quickly. This is something that human physicians, sadly, cannot do themselves (or at least, they can’t do it with nearly the accuracy or efficiency). The system looked at the woman’s genetic information and compared it to 20 million clinical oncology studies. After doing so, it determined that the patient had an exceedingly rare form of leukemia.
Accuracy, however, isn’t the only priority for Stanford’s AI system. The team is also working towards making this technology accessible via smartphone so that even those with limited healthcare availability can get the help they need.
“My main eureka moment was when I realized just how ubiquitous smartphones will be. Everyone will have a supercomputer in their pockets with a number of sensors in it, including a camera. What if we could use it to visually screen for skin cancer? Or other ailments?” ” said Esteva.
These researchers are busy refining the algorithm and trying to better understand how it makes decisions. But hopefully soon, this potentially life-saving technology will be available for all with a smartphone. And, in the future, if this technology is adapted for other ailments or purposes, the future of healthcare could be bright even for those who cannot afford insurance. This could, in the long run, save many, many lives.
Wouldn’t it be wonderful if the need for chemotherapy no longer existed? In some cases, these treatments aren’t even effective enough to send patients into remission, but for many people, there are few other options.
What if there was an easier and more effective way to tackle cancer? Thanks to one recent case, there is.
Doctors at London’s Great Ormond Street Hospital recently announced that they successfully cured two babies of leukemia, when their previous treatments failed. This was also the first attempt in the world to treat cancer with genetically engineered immune cells provided by a donor. This case is published in the journal Science Translational Medicine.
Currently, there are two methods of administering genetically engineered immune cells into a human body. The first approach, an “off-the-shelf” approach, was used by the doctors at London’s Great Ormond Street Hospital. In this approach, engineered T-cells are modified to become ‘one size fits all’ for cancer patients. The patient is hooked up to an IV, and these modified cells are dripped into their veins whenever needed. The second approach involves collecting a cancer patient’s blood cells, engineering them, then dripping them back in, again through an IV.
The second approach is primarily used by companies like Juno Therapeutics and Novartis. It costs millions of dollars and requires a large logistical effort, so the first approach that uses universal immune cells seems more practical. But there was significant doubt placed on the London doctors and their ability to cure the babies using this method. Additionally, the babies were on a standard chemotherapy regimen before the experiment, which has given some people doubt whether the successful treatment was the engineered T-cells, the chemotherapy, or perhaps both.
If the “off-the-shelf” approach did cure the infants, it could potentially save millions of lives. Doctors could collect blood from a donor, disperse it into hundreds of doses, then freeze and store it for $4,000 per dose. This is an affordable option compared to the second approach which costs $50,000 to alter a patient’s cells and return them.
This could be considered the singular cure for leukemia. T-cells assist the immune system by attacking leukemic cells, a theoretically simple and effective solution. Treatments that involve these engineered T-cells, like the nicknamed “off-the-shelf” approach, are known as CAR-T cell therapy, although they are not yet sold commercially. Juno Therapeutics and Novartis have previously conducted studies, finding that CAR-T cell therapy cured about half of all patients involved.
“The patient could be treated immediately, as opposed to taking cells from a patient and manufacturing them,” said Julianne Smith, vice president of CAR-T development for Cellectis, which specializes in the supply of universal cells. Still, others side with the notion that treatments should use only the patient’s own cells, not someone else’s. But whatever side of the debate you are on, all could agree that if either is proven as an effective life-saving treatment, it should become an available option for patients. Being both relatively affordable and possibly more effective than current conventional approaches, this could be the future of alternative cancer treatments.
Here’s some much needed good news to usher in the new year –cancer deaths have dropped 25 percent in 20 years in the United States. To put this figure into context, that’s 2.1 million less cancer-related deaths between 1991 to 2014.
The report is based on Cancer Statistics 2017, an annual report on cancer incidence, mortality, and survival, released by the American Cancer Society. In 1991, death rates due to cancer peaked, reaching 215.1 (per 100,000 population), which significantly dropped in 2014 (the latest year available for analysis) to 161.2 (per 100,000 population).
Lung cancer remains the leading cause of cancer death in the US, for both men and women. Nevertheless, the condition saw a 43 percent decline from 1991 to 2014. Deaths from breast cancer were down 38 percent from 1989 to 2014; while prostate cancer was down 51 percent from 1993 to 2014; and colorectal cancer was down 51 percent from 1976 to 2014.
Despite these improved mortality statistics, “lung, colorectal, prostate, and breast cancers continue to be among the most common causes of cancer death, accounting for about 46% of the total cancer deaths among men and women. More than 1 out of every 4 cancer deaths is due to lung cancer,” Cancer.org writes in a press release.
Continuing the Fight Against Cancer
Declining rates in lung cancer can be credited to more and more people making a concerted effort to quit smoking. However, rates were shown to be declining twice as fast in men versus women, which could likely be due to more women taking up smoking years after men.
For prostate cancer, over diagnosing caused by the PSA blood tests has also been reduced, which could equate to lower incidence. Colonoscopies, a method of pre-screening and removal for pre-cancerous polyps (that typically lead to colorectal cancer) have aided in reducing colorectal cancer. While death rates for this particular type of cancer went down overall, the research notes that they went up among people younger than 50 years (at a rate of two percent per year from 1993 to 2013).
These figures highlight that we are indeed making slow, but steady progress in this fight against cancer. And if anything, they just give us a renewed focus on finding a viable treatment for the 1,688,780 new cancer cases the organization projects will occur in 2017. From that number, an estimated 600,920 people will still lose their battle against the deadly disease.
Obviously our fight against cancer is far from over. But as the Chief Medical Officer of the American Cancer Society, Otis W. Brawley, MD, FACP, points out:
The continuing drops in the cancer death rate are a powerful sign of the potential we have to reduce cancer’s deadly toll. Continuing that success will require more clinical and basic research to improve early detection and treatment, as well as creative new strategies to increase healthy behaviors nationwide. Finally, we need to consistently apply existing knowledge in cancer control across all segments of the population, particularly to disadvantaged groups.
Cancer research is an area of medical science that, rightfully, gets considerable attention. There are nearly 14.5 million Americans with a history of cancer and with more than 13 million estimated new cancer cases each year. It’s no wonder even artificial intelligence (AI) has gotten into the field. Researchers from the University of Michigan are not getting left behind, with a groundbreaking method that has the potential to eliminate tumors.
This new technology uses nano-sized discs, about 10 nm to be exact, to teach the body to kill cancer cells. “We are basically educating the immune system with these nanodiscs so that immune cells can attack cancer cells in a personalized manner,” said James Moon from the University of Michigan.
Each of these ‘nanodiscs’ is full of neoantigens (tumor-specific mutations) that teach the immune system’s T-cells to recognize each neoantigen and kill them. These work hand-in-hand with immune checkpoint inhibitors that boost the responses of T-cells — forming an anti-cancer system in the body that wipes out tumors and potentially keeps them from reemerging.
“The idea is that these vaccine nanodiscs will trigger the immune system to fight the existing cancer cells in a personalized manner,” Moon added. The study is published in the journal Nature Materials.
So far, the nanodiscs were successfully tested on mice and were shown to be rather promising, eliminating tumors in 10 days. These were also able to shut down identical tumors in the mice after being reinserted 70 days later. “This suggests the immune system ‘remembered’ the cancer cells for long-term immunity,” said Rui Kuai, lead author of the study.
Of course, it’s going to be a long while before this designer vaccine rolls out for public use. The researchers still need to scale it up for tests on larger animals. It will then take even more time before it can actually be tested on human beings.
When we think of cancer surgery, we often imagine surgeons with a scalpel removing tumors. But there’s another way to remove tumors — laser surgery.
There are three kinds of laser surgery treatments. Carbon dioxide lasers treat cancers on the skin or those deep in organ tissue; dye lasers work a little deeper, up to less than three millimeters of tissue; and for even deeper jobs, surgeons use Nd:YAG lasers, which reach the targeted part of the body via fiber optic cable.
Dr. Vincent Ansanelli, who is a breast cancer surgeon at Laser Breast Cancer Surgery in Long Island, is one of the doctors pioneering treatment (and saving lives) using a carbon dioxide laser. With this method, when the laser comes into contact with human tissue, it literally causes the tissue to vaporize. In an interview, Ansanelli notes the benefits of this, saying that, when used in animal studies, the local recurrence rate with the carbon dioxide method was some 30% less than normal.
The laser isn’t just dissecting, it’s destroying tumor cells.
Laser surgeries as a whole are used to treat a wide variety of cancers. They’re commonly used in early cancers close to the skin, like cervical or penile cancer. They are also used in cancers affecting organ linings, such as that of the esophagus or the windpipe. Further, they can even be used in some kinds of lung cancer.
Whichever method is used, laser surgeries have many benefits. To being with, they are more accurate. Lasers seal blood and lymph vessels, limiting bleeding, swelling, and the spread of cancer cells. The heat sanitizes the site, further limiting spread. Only local anesthesia is needed for this kind of surgery, and is often done in an outpatient basis.
While these laser methods are allowing us to fight cancer and keep it away as never before, there are a host of other developments that are helping us wage a better war on this lethal disease.
Advances in medicine have spurred many new hopes for both treatment and a cure. These include better diagnosis and better treatment of the disease. Better biological understanding of cancer has allowed us to pinpoint proteins and other chemicals essential to the spread of the disease. This helps us target these chemicals, stymieing cancer’s spread.
Nanoparticle and mini robot treatments are being developed that target cancer cells with a degree of accuracy not possible with a scalpel or chemo. This targeted approach removes most, if not all traces of the cells.
AI has also been trying to work its magic to end cancer. AI seems promising in cancer prevention since it can crunch patient files and research papers in far less time than a doctor. There is no bullet to cancer; all these are just pieces to the puzzle. Ultimately, it will take more funding and research for us to cure “the Big C.”
Cancer is still a scourge for humankind. According to the American Cancer Society, more than 14.1 million people have cancer worldwide, and it’s expected to grow to 21.7 million by 2030, bringing with it 13 million expected deaths. While a substantial portion of cancer causing factors can be avoided, the problem persists due to both lifestyle choices and environmental causes.
Tech billionaire Sean Parker, with his Parker Institute for Cancer Immunotherapy, is one of those who are determined to bring an end to this disease. An existing research partnership between six research universities and cancer centers is about to get a boost. Just this week, Parker’s institute announced that it will start working with the Cancer Research Institute (CRI) in order to uncover genetic tumor markers called neoantigens using predictive algorithms and bioinformatics.
The partnership is comprised of 30 organizations, including prestigious groups like the Broad Institute of MIT and Harvard, Caltech, the Dana-Farber Cancer Institute, and the Washington University School of Medicine.
The Answer to Cancer?
Neoantigens are said to be genetic markers found only in tumors and are specific to individuals. These are perfect for new immunotherapy treatments, presenting “an important first step in accelerating immunotherapy research,” said Ramy Ibrahim, VP of clinical development at the Parker Institute.
The partnership would work to “test and continually improve the mathematical algorithms they use to analyze tumor DNA and RNA sequences in order to predict the neoantigens that are likely to be present on each patient’s cancer and most visible to the immune system,” according to CRI. These predictive algorithms will be managed and analyzed by open science nonprofit, Sage Bionetworks.
Each participating organization will study specific gene sequences from both cancerous and non-cancerous tissues, determining which ones are recognizable by T-cells. Once enough data is gathered, it can lead to producing more effective personalized neoantigen vaccines for cancer, says CRI.
As Robert D. Schreiber of Washington University School of Medicine in St. Louis says: “We believe that this type of precision medicine, used alone or with other forms of immunotherapy, will significantly improve our capacity to treat cancer patients more effectively and with fewer side effects than current treatments.”