Tagged: Cancer Toggle Comment Threads | Keyboard Shortcuts

  • richardmitnick 3:31 pm on April 21, 2016 Permalink | Reply
    Tags: , Cancer, Mapping Cancer Markers project,   

    From Mapping Cancer Markers at WCG: “Mapping Cancer Markers Now Examining Ovarian Cancer” 

    New WCG Logo
    WCGLarge

    21 Apr 2016
    The Mapping Cancer Markers research team

    Summary
    The Mapping Cancer Markers project now includes markers for the most common form of ovarian cancer, with a goal to understand the how this disease progresses from early-stage to late-stage.

    The Mapping Cancer Markers project, which had been concentrating on lung cancer, now includes work units related to ovarian cancer. The researchers are seeking to identify the genes that are important in differentiating between early-stage and late-stage ovarian cancer.

    The Goals of Mapping Cancer Markers

    Cancer is caused by genetic or environmental changes that interfere with biological mechanisms that control cell growth. These changes can be detected in tissue samples through the presence of their unique chemical indicators, such as DNA and proteins, which together are known as “markers.” Specific combinations of these markers may be associated with a given type of cancer. Additionally, the pattern of markers can determine whether an individual is susceptible to developing a specific form of cancer, and may also predict the progression of the disease, helping to suggest the best treatment for a given individual. In order to identify these markers, the project is analyzing millions of data points collected from thousands of healthy and cancerous patient tissue samples.

    Why Ovarian Cancer?

    Around the world, nearly 250,000 women are diagnosed with ovarian cancer each year, and it is responsible for 140,000 deaths each year. Statistics show that just 45 percent of women with ovarian cancer survive for five years. The main types of ovarian cancer are epithelial, germ cell and stromal cell, with the epithelial type accounting for roughly 85-90 percent of all cases. Ovarian cancer often goes undetected in early stages due to the disease being confined to the ovary, the subtlety of the symptoms, and the lack of an effective screening tool. Therefore, most presentations of the disease are detected in late stages or once the cancer has spread outside the ovary, making treatment less effective and less likely to succeed. It is for these reasons that we have chosen epithelial ovarian cancer as our next area of study.

    Understanding the Progression of Ovarian Cancer

    In the next stage of Mapping Cancer Markers, we will attempt to identify important genes in defining the differences between early and late-stage cancers. There is a strong correlation between survival time and cancer stage; patients with early-stage cancer tend to have longer lives. We will be using a curated database of ovarian cancer survival data developed by researchers around the world as a starting point.

    For the purposes of this study, we are defining early-stage death as before three years after diagnosis, and late-stage death as more than four years after diagnosis. We are looking for the genes that are important in differentiating between these two classes of ovarian cancer to allow us to understand the underlying mechanisms of how cancer progresses.

    As compared to the earlier work of Mapping Cancer Markers, where we studied lung cancer, this phase will have a larger and more complex dataset. We estimate that the number of “experiments” we can perform within a single work unit will be much less, as each experiment will take longer to solve. Although the dataset is larger, that means that we are able to use our algorithm against many more points of data, which will hopefully return a very clear result.

    We thank the thousands of World Community Grid volunteers who have supported this project since its launch in 2013, and look forward to continuing to work with you as our research progresses.

    See the full article here.

    Please help promote STEM in your local schools.
    STEM Icon

    Stem Education Coalition

    World Community Grid (WCG) brings people together from across the globe to create the largest non-profit computing grid benefiting humanity. It does this by pooling surplus computer processing power. We believe that innovation combined with visionary scientific research and large-scale volunteerism can help make the planet smarter. Our success depends on like-minded individuals – like you.”

    WCG projects run on BOINC software from UC Berkeley.

    BOINC is a leader in the field(s) of Distributed Computing, Grid Computing and Citizen Cyberscience.BOINC is more properly the Berkeley Open Infrastructure for Network Computing.

    BOINC WallPaper

    CAN ONE PERSON MAKE A DIFFERENCE? YOU BET!!

    “Download and install secure, free software that captures your computer’s spare power when it is on, but idle. You will then be a World Community Grid volunteer. It’s that simple!” You can download the software at either WCG or BOINC.

    Please visit the project pages-

    Help Stop TB
    WCG Help Stop TB
    Outsmart Ebola together

    Outsmart Ebola Together

    Mapping Cancer Markers
    mappingcancermarkers2

    Uncovering Genome Mysteries
    Uncovering Genome Mysteries

    Say No to Schistosoma

    GO Fight Against Malaria

    Drug Search for Leishmaniasis

    Computing for Clean Water

    The Clean Energy Project

    Discovering Dengue Drugs – Together

    Help Cure Muscular Dystrophy

    Help Fight Childhood Cancer

    Help Conquer Cancer

    Human Proteome Folding

    FightAIDS@Home

    World Community Grid is a social initiative of IBM Corporation
    IBM Corporation
    ibm

    IBM – Smarter Planet
    sp

     
  • richardmitnick 6:20 pm on April 17, 2016 Permalink | Reply
    Tags: , Cancer,   

    From Nature: “Cocktails for cancer with a measure of immunotherapy” 

    Nature Mag
    Nature

    13 April 2016
    Heidi Ledford

    1
    Some cancer drugs (pictured here, dried adriamycin viewed under a microscope) might work better when paired with immunotherapies. Margaret Oechsli

    In cancer research, no success is more revered than the huge reduction in deaths from childhood leukaemia. From the 1960s to the 2000s, researchers boosted the number of children who survived acute lymphoblastic leukaemia from roughly 1 in 10 to around 9 in 10.

    What is sometimes overlooked, however, is that these dramatic gains against the most common form of childhood cancer were made not through the invention of new drugs or technologies, but rather through a reassessment of the tools in hand: a dogged analysis of the relative gains from different medicines and careful strategizing over how best to apply them side by side as combination therapies.

    2
    Cancer-fighting viruses win approval Killer T cells (orange) are recruited to attack malignant cells (mauve) in the viral-based cancer therapy T-VEC. Dr. Andrejs Liepins/SPL

    “It wasn’t just about pounding drugs together,” says Jedd Wolchok, a medical oncologist at Memorial Sloan Kettering Cancer Center in New York City. “It was about understanding the mechanism and figuring out what should be given when.”

    That lesson has particular relevance in cancer research today. A new class of immunotherapies — which turn the body’s immune system against cancerous cells — is elevating hopes about combination therapies again. The drugs, called checkpoint inhibitors, have already generated great excitement in medicine when applied on their own. Now there are scores of trials mixing these immune-boosting drugs with one another, with radiation, with chemotherapies, with cancer-fighting viruses, with cell treatments and more. “The field is exploding,” says Crystal Mackall, who leads the paediatric cancer immunotherapy programme at Stanford University in California.

    Fast-moving trends in cancer biology often fail to meet expectations, and little is yet known about how these drugs work together. Some observers warn that the combinations being tested are simply marriages of convenience — making use of readily available compounds or capitalizing on business alliances. “In many cases, we’re moving forward without a rationale,” says Alfred Zippelius, an oncologist at the University of Basel in Switzerland. “I suspect we’ll see some disappointment in the next few years with respect to immunotherapy.”

    But many clinicians argue that delay is not an option as their patients queue up for the next available clinical trial. “Right now I have more patients that could benefit from combinations than there are combinations being tested,” says Antoni Ribas, an oncologist at the University of California, Los Angeles. “We’re always waiting on the next slot.”

    Lying in wait

    Immunotherapies have been more than a century in the making, starting when physicians first noticed mysterious remissions in a few people with cancer who contracted a bacterial infection. The observations led to a hypothesis: perhaps the immune system is able to kill tumours when made hypervigilant by an infection. The concept has vast appeal. What better way to beat a fast-evolving biological system such as a tumour than with a fast-evolving biological immune system? But it took decades for researchers to turn that observation into something useful.

    3
    Immune cells boost cancer survival from months to years. Therapies that make use of a patient’s own T cells, a component of the immune system, are showing promise in the clinic. David Scharf/Corbis

    Part of the trouble, they eventually learned, is that tumours suppress the immune response. T cells, the immune system’s weapon of choice against cancer, would sometimes gather at the edge of a tumour and then just stop.

    It turned out that a class of molecules called inhibitory checkpoint proteins was holding those T cells at bay. These proteins normally protect the human body from unwarranted attack and autoimmunity, but they were also limiting the immune system’s ability to detect and fight tumours.

    In 1996, immunologist James Allison, now at the University of Texas MD Anderson Cancer Center in Houston, showed that switching off a checkpoint protein called CTLA-4 helped mice to fend off tumours. The discovery suggested that there was a way to re-mobilize T cells and beat cancer.

    In 2011, the US Food and Drug Administration (FDA) approved the first checkpoint inhibitor — a drug, called ipilimumab, that inhibits CTLA-4 — to treat advanced melanoma. The improvements were modest: about 20% of patients benefited from ipilimumab, and the survival gain was less than four months on average. But a handful of recipients are still alive a decade after starting the therapy — a stark contrast with most new cancer drugs, which often benefit more patients in the short term, but don’t have a durable response (see ‘Desperately seeking survival‘).

    Ipilimumab was at the leading edge of a flood of checkpoint inhibitors to enter clinical trials. The drug’s developer, Bristol-Myers Squibb of New York, followed up with the approval of nivolumab, which inhibits the protein PD-1. And a host of other companies have jumped into the immunotherapy fray, as have academics such as Edward Garon at the University of California, Los Angeles. “Our group gladly shifted into this,” says Garon, who began focusing on checkpoint inhibitors in 2012. “It was very clear this was going to have a major impact.”

    But even as the family of checkpoint inhibitors was rapidly expanding, the drugs were running up against the same frustrating wall: only a minority of patients experienced long-lasting remission. And some cancers — such as prostate and pancreatic — responded poorly, if at all, to the drugs.

    4
    Therapeutic cancer vaccine survives biotech bust. Therapeutic cancer vaccines harness the patient’s own immune system to fight tumours. Rolf Ritter/Cultura Science/Getty

    Further research revealed a possible explanation: many people who were not responding well to the drugs were starting the treatment without that phalanx of T cells waiting at the margins of their tumours. (In the lingo of the field, their tumours were not inflamed.) Researchers reasoned that if they could raise this T-cell response first, and recruit the cells to the edges of the tumour, they might get a better result with the checkpoint inhibitors.

    That realization fuelled a rush to test combinations of drugs (see ‘Combinatorial explosion’). Radiation and some chemotherapies kill enough tumour cells to release proteins that the immune system might then recognize as foreign and attack. Vaccines containing these proteins, called antigens, could have a similar effect. “On some level, one can make an argument for almost any drug combining well with an immunotherapy,” says Garon. “And obviously we know not all of them will.”

    Mixing it up

    One of the first combinations to be tested was made up of two immunotherapies — ipilimumab and nivolumab — at once. Although the targets of these drugs both do the same job, silencing T cells, they do so in different ways: CTLA-4 prevents the activation of T cells; PD-1 blocks the cells once they have infiltrated the tumour and its environment. And treating mice with compounds that block both proteins yielded a more-inflamed tumour as well3. “There was reason to think that if you block both, the T cells will be even more ready to kill the tumours,” says Michael Postow, an oncologist at Memorial Sloan Kettering.

    Together, ipilimumab and nivolumab boost response rates in people with advanced melanoma from 19% with just ipilimumab to 58% with the combination. The combination also produces more-dangerous side effects than using either drug alone, but physicians are learning how to treat immunotherapy reactions, says Postow.

    5

    Ipilimumab generally doesn’t help people with lung cancer when given on its own, but researchers are now testing it with nivolumab. Normally, they would not have bothered to investigate a combination involving a drug that had failed on its own, Garon says.

    The new approach is grounded in immunology, but some researchers worry that the effort could be wasted, he adds. Researchers are also testing inhibitors of other checkpoint proteins, including TIM-3 and LAG-3, in combination with those that block PD-1.

    6
    Cancer treatment: The killer within. Illustration by Brendan Monroe

    The combination approach is breathing life into drugs that had been shelved. For example, a protein called CD40 stimulates immune responses and has shown promise against cancer in animals. But in the wake of disappointing early clinical trials, some companies put their CD40 drugs to the side.

    Years later, mouse studies showed that combining CD40 drugs with a checkpoint inhibitor could boost their effect. Now, at least seven companies are developing them. Cancer immunologists have listed the protein as one of the targets they are most interested in studying, says Mac Cheever, a cancer immunologist at the Fred Hutchinson Cancer Research Center in Seattle, Washington.

    Cancer vaccines — long pursued by researchers but burdened by repeated failures in clinical trials — may also see a renaissance. There are now more than two dozen trials of cancer vaccines that make use of a checkpoint inhibitor.

    Some promising combinations have been uncovered by serendipitous clinical observations. Researchers at Johns Hopkins University in Baltimore, Maryland, were conducting trials of epigenetic drugs, which alter the chemical tags on chromosomes. They shifted a handful of people with lung cancer who had not responded to the drugs to a clinical trial of nivolumab. Five of them responded — a much higher proportion than expected. The discovery became the seed for an ongoing clinical trial launched in 2013 to study combinations of epigenetic drugs and immunotherapies. Preclinical work has now provided evidence that epigenetic drugs can affect aspects of the immune response.

    Riding the wave

    These chance observations could lead to real advances, says Wolchok. “We’re riding the wave of enthusiasm.” But extracting the most from these combinations will require more well-designed preclinical studies to support the human ones. Just as attention to combinations of chemotherapies fuelled advances in treating paediatric leukaemias, the current combinatorial craze will require careful planning to work out the right pairings and timing of therapies.

    7
    Personalized cocktails vanquish resistant cancers. Lung cancer cells are cultured and challenged with an array of drugs in a proposed strategy to overcome treatment resistance. Steve Gschmeissner/Science Photo Library

    Another class of drug, known as targeted therapies, could also receive a significant boost from immunotherapy. These drugs, which target proteins bearing specific mutations, generate a high response rate when given to patients with those mutations, but the tumours often develop resistance to the drugs and come roaring back. Coupling targeted therapies with a checkpoint inhibitor, researchers reason, could yield both high response rates and durable remissions.

    One of the first targeted therapies for melanoma was an inhibitor that is specific to certain mutations in BRAF proteins that can drive tumour growth. However, an early attempt to combine this drug with ipilimumab was aborted when trial participants showed signs of possible liver damage5. No one was injured, but for some it was an important reminder that combinations can yield unanticipated side effects. “It was a good lesson for us to learn,” says Wolchok. “It will not be as simple as we imagined.”

    Paying careful attention to sample collection during clinical trials would help researchers to catch toxicity problems early, says Jennifer Wargo, a cancer researcher at MD Anderson. “We’re making mistakes by looking just at clinical endpoints,” she adds. “We need to be smarter about how we run these trials.”

    In one of his latest trials, Wolchok wants to combine immunotherapy with a drug that targets a cellular pathway that some cancer cells use to maintain their rapid division. Cancers with mutations in this pathway, which is regulated by the protein MEK, can be extraordinarily difficult to treat.

    8
    Cancer therapy: an evolved approach. Tumour cells can evolve resistance to chemotherapy drugs such as oxaliplatin, shown under a microscope. Margaret Oechsli.

    But the pathway is also important for T-cell development, so Wolchok is working to determine the right timing for the treatment. One approach could be to use a MEK inhibitor to quiet tumours in mice and to release tumour antigens. He would then wait for the T-cell response to rejuvenate before adding the immunotherapy. “You want to make sure you’re not trying to activate the immune system at the same time you’re turning off that signalling,” he says.

    Garon is watching such trials with optimism, but he’s aware that there may be a limit to how well combinations will perform. He sees a cautionary tale in a drug from an earlier era that works mainly in people with a mutation in the protein EGFR. Researchers spent a decade trying to find drugs that could turn a non-responding patient into a responder. “It is now clear that there probably is no such agent,” he says. “I’m hopeful we won’t be repeating that same response, but we have to watch our data cautiously.”
    Data frenzy

    Researchers are so ravenous for those data that the results are being unveiled at major meetings at an earlier stage than in the past, he adds. “People are getting up and presenting response rates when the number treated is five,” Garon says. “We generally have had a higher threshold than that.” He worries that presenting such early data could prompt community physicians in the audience to start making decisions on treatments before they are appropriately studied.

    The excitement is also fuelling a frenzy of clinical trials that are often based on speed rather than rationale. “Right now I’m kidding myself if I say I’m picking a combination because I have a scientific reason to pick it,” says Mackall. “It’s likely to just be what was available.”

    9
    Laguna Design/SPL

    The strategy may still produce some wins. “There is plenty of opportunity for serendipity now,” says Robert Vonderheide, who studies CD40 at the University of Pennsylvania in Philadelphia. But as the field matures, he says, this could give way to a more-systematic approach, similar to the careful planning and testing of variables used for paediatric leukaemias.

    Despite his concerns, Garon is excited to be a part of the immunotherapy wave. Last autumn, he and his colleagues held a banquet for the patients who had been enrolled in his first immunotherapy trials three years earlier. These were the lucky survivors — the few who had shown a dramatic response. As he looked around the table at the guests of honour, he marvelled at their recovery. All had been diagnosed with advanced lung cancer, and many had been too weak to work. Now they were talking about their families, re-embarking on careers and taking up old hobbies such as golf and running. “We’ve never been able to hold a banquet like that before,” he says. “I would love to hold many more.”

    See the full article here .
    http://www.nature.com/news/cocktails-for-cancer-with-a-measure-of-immunotherapy-1.19745

    Please help promote STEM in your local schools.

    STEM Icon

    Stem Education Coalition

    Nature is a weekly international journal publishing the finest peer-reviewed research in all fields of science and technology on the basis of its originality, importance, interdisciplinary interest, timeliness, accessibility, elegance and surprising conclusions. Nature also provides rapid, authoritative, insightful and arresting news and interpretation of topical and coming trends affecting science, scientists and the wider public.

     
  • richardmitnick 5:08 pm on April 17, 2016 Permalink | Reply
    Tags: , Cancer, Cancerous Coconspirators: Tumor Cells That Travel Together Spread Cancer,   

    From SA: “Cancerous Coconspirators: Tumor Cells That Travel Together Spread Cancer” 

    Scientific American

    Scientific American

    April 1, 2016
    Viviane Callier

    1
    Credit: COURTESY OF BREANNA MOORE Cheung Laboratory, Fred Hutchinson Cancer Research Center

    Metastasis is behind the vast majority of cancer deaths: when cancer cells break away from a tumor and lodge in new places, the disease becomes harder to treat. A new study shows that, contrary to expectations, most metastatic tumors are seeded not by single cells from the primary tumor but by clusters of diverse cancer cells that leave in a group and travel through the bloodstream together. The cells in these circulating clusters communicate with one another and produce specific proteins that could be used as drug targets or biomarkers for risk of metastasis.

    To determine how metastases form, cancer cell biologist Andrew Ewald and his team at Johns Hopkins University created tumors in mice by injecting a mixture of multicolored cancer cells into the rodents’ mammary glands. If tumors originated elsewhere from single cells, then they would show up under the microscope as one uniform color. If instead tumors were seeded by clusters of cells, then they would grow into rainbow-colored balls. The team found that about 95 percent of the cancers that formed were in fact multicolored and therefore derived from multiple cells (lung metastasis, above).

    In a second experiment, the researchers examined hundreds of cancerous cells grown together in a petri dish but placed so that they were not touching. Almost all of them died. In contrast, cells in another dish that were aggregated into clusters subsequently formed more colonies—even though there were fewer “seeds” to begin with. “Controlling for cell number, there is more than a 100-fold increase in efficiency of metastasis formation in the aggregated cells,” Ewald says. The findings were published* in February in the Proceedings of the National Academy of Sciences USA.

    It is not yet entirely clear why the aggregated cells survive and metastasize more effectively, but it is likely that cooperation among tumor cells within clusters—for example, exchanging signaling molecules—protects against cell death in the bloodstream or at distant sites, explains Joan Brugge, a cancer cell biologist at Harvard Medical School who was not involved in the study.

    As for potential benefits to patients, Ewald’s team also found that the traveling clusters share molecular features and nearly all make the protein keratin 14. “We could potentially use this [insight] to develop targeted ways to attack all the metastatic cells,” Ewald says. The idea would be to wipe out those cells wherever they are in the body, whether or not they are proliferating—a different approach from most standard therapies, which focus on attacking rapidly proliferating cells but not the circulating, invasive ones that initiate secondary cancers.

    *Science paper:
    Polyclonal breast cancer metastases arise from collective dissemination of keratin 14-expressing tumor cell clusters

    See the full article here .

    Please help promote STEM in your local schools.

    STEM Icon

    Stem Education Coalition

    Scientific American, the oldest continuously published magazine in the U.S., has been bringing its readers unique insights about developments in science and technology for more than 160 years.

     
  • richardmitnick 7:17 am on April 14, 2016 Permalink | Reply
    Tags: , Cancer,   

    From UCLA: “Microscope uses artificial intelligence to find cancer cells more efficiently” 

    UCLA bloc

    UCLA

    April 13, 2016
    Shaun Mason

    Device invented by UCLA professor uses deep learning and photonic time stretch to analyze 36 million images per second.

    Scientists at the California NanoSystems Institute at UCLA have developed a new technique for identifying cancer cells in blood samples faster and more accurately than the current standard methods.

    In one common approach to testing for cancer, doctors add biochemicals to blood samples. Those biochemicals attach biological “labels” to the cancer cells, and those labels enable instruments to detect and identify them. However, the biochemicals can damage the cells and render the samples unusable for future analyses.

    There are other current techniques that don’t use labeling but can be inaccurate because they identify cancer cells based only on one physical characteristic.

    1
    Photonic time stretch microscope. Tunde Akinloye/CNSI

    The new technique images cells without destroying them and can identify 16 physical characteristics — including size, granularity and biomass — instead of just one. It combines two components that were invented at UCLA: a photonic time stretch microscope, which is capable of quickly imaging cells in blood samples, and a deep learning computer program that identifies cancer cells with over 95 percent accuracy.

    Deep learning is a form of artificial intelligence that uses complex algorithms to extract meaning from data with the goal of achieving accurate decision making.

    The study, which was published* in the journal Nature Scientific Reports, was led by Barham Jalali, professor and Northrop-Grumman Optoelectronics Chair in electrical engineering; Claire Lifan Chen, a UCLA doctoral student; and Ata Mahjoubfar, a UCLA postdoctoral fellow.

    Photonic time stretch was invented by Jalali, and he holds a patent for the technology. The new microscope is just one of many possible applications; it works by taking pictures of flowing blood cells using laser bursts in the way that a camera uses a flash. This process happens so quickly — in nanoseconds, or billionths of a second — that the images would be too weak to be detected and too fast to be digitized by normal instrumentation.

    The new microscope overcomes those challenges using specially designed optics that boost the clarity of the images and simultaneously slow them enough to be detected and digitized at a rate of 36 million images per second. It then uses deep learning to distinguish cancer cells from healthy white blood cells.

    “Each frame is slowed down in time and optically amplified so it can be digitized,” Mahjoubfar said. “This lets us perform fast cell imaging that the artificial intelligence component can distinguish.”

    Normally, taking pictures in such minuscule periods of time would require intense illumination, which could destroy live cells. The UCLA approach also eliminates that problem.

    “The photonic time stretch technique allows us to identify rogue cells in a short time with low-level illumination,” Chen said.

    The researchers write in the paper that the system could lead to data-driven diagnoses by cells’ physical characteristics, which could allow quicker and earlier diagnoses of cancer, for example, and better understanding of the tumor-specific gene expression in cells, which could facilitate new treatments for disease.

    The study’s other authors were Li-Chia Tai, Ian Blaby and Allen Huang of UCLA, and Kayvan Niazi of NantBio. The research was supported by NantWorks, LLC, the parent company of NantBio.

    Science paper:
    Deep Learning in Label-free Cell Classification

    Science team and affiliations:

    Department of Electrical Engineering, University of California, Los Angeles, California 90095, USA
    Claire Lifan Chen, Ata Mahjoubfar, Allen Huang & Bahram Jalali
    California NanoSystems Institute, Los Angeles, California 90095, USA
    Claire Lifan Chen, Ata Mahjoubfar, Li-Chia Tai, Kayvan Reza Niazi & Bahram Jalali
    Department of Chemistry and Biochemistry, University of California, Los Angeles, California 90095
    Ian K. Blaby
    NantWorks, LLC, Culver City, California 90232, USA
    Kayvan Reza Niazi
    Department of Bioengineering, University of California, Los Angeles, California 90095, USA
    Kayvan Reza Niazi & Bahram Jalali
    Department of Surgery, David Geffen School of Medicine, University of California, Los Angeles, California 90095, USA
    Bahram Jalali

    Contributions

    C.L.C., A.M. and B.J. conceived the classification method. C.L.C., A.M. and B.J. designed the TS-QPI system and the machine learning pipelines. A.M. and C.L.C. performed experiments, collected the data, and processed the signals. C.L.C. and A.M. coded the image processing and the machine learning algorithms. A.M., L.C.T., A.H. and C.L.C. designed and fabricated the microfluidic channels. K.R.N. provided SW-480 and OT-II cell samples. I.K.B. provided algal cell samples. C.L.C., A.M., B.J. and K.R.N. analyzed the results. C.L.C., A.M., B.J., I.K.B. and K.R.N. prepared the manuscript. B.J. supervised all aspects of the work.

    See the full article here .

    Please help promote STEM in your local schools.

    STEM Icon

    Stem Education Coalition

    UC LA Campus

    For nearly 100 years, UCLA has been a pioneer, persevering through impossibility, turning the futile into the attainable.

    We doubt the critics, reject the status quo and see opportunity in dissatisfaction. Our campus, faculty and students are driven by optimism. It is not naïve; it is essential. And it has fueled every accomplishment, allowing us to redefine what’s possible, time after time.

    This can-do perspective has brought us 12 Nobel Prizes, 12 Rhodes Scholarships, more NCAA titles than any university and more Olympic medals than most nations. Our faculty and alumni helped create the Internet and pioneered reverse osmosis. And more than 100 companies have been created based on technology developed at UCLA.

     
  • richardmitnick 6:58 am on April 14, 2016 Permalink | Reply
    Tags: , Cancer,   

    From UCLA: “Experimental therapy for brain cancer developed by UCLA and Caltech could prevent drug resistance” 

    UCLA bloc

    UCLA

    April 13, 2016
    Reggie Kumar

    1
    Information from penny-sized microfluidic chips allowed researchers to anticipate resistance to cancer treatment.

    UCLA and Caltech researchers have developed a technique that shows promise for preventing drug resistance in people with glioblastoma, the most common and deadliest type of brain cancer.

    Drug resistance is one of the primary obstacles in treating glioblastoma — it is extremely common and affects virtually all people with the disease. But there is no consensus on why the body stops responding to treatment after a period of time, and scientists don’t yet have a tool for predicting drug resistance during the early stages of treatment.

    The new technique uses penny-sized microfluidic chips that are equipped with minuscule DNA “bar codes,” which are no bigger than a single cell.

    Glioblastoma tumors can grow rapidly and spread throughout the brain. The aggressive behavior is triggered by genetic mutations that cause the tumor cells’ protein signaling networks to become overly active. As a result, glioblastoma cells continuously receive signals that make them grow, divide and invade healthy tissue in the brain.

    The current treatments for glioblastoma are designed to disrupt specific elements of the protein networks and to block the signaling that powers the tumor cells. But even when that approach is successful, it usually only works for a short time before the body becomes resistant to the treatment.

    A paper about the new approach was published in the journal Cancer Cell. The research was led by James Heath, co-director of the UCLA Jonsson Comprehensive Cancer Center’s Nanotechnology Program. Heath and his team looked at how glioblastoma responded to a drug called CC214-2, which targets a signaling protein called mTOR. Mice with glioblastoma initially responded to CC214-2, but after a month they started to resist the drug, and their tumors began to grow again.

    The researchers collected information from the microfluidic chips, which allowed them to anticipate resistance from a single or combination cancer treatment. They also found that within only two days after administering CC214-2, the cancer cells were adapting to the drug, and their ability to adapt foreshadowed full-scale drug resistance.

    The cancer cells’ response to the drug was analogous to how automobile traffic responds to a road closure — they simply found new molecular routes through which to maintain their hyperactive signaling. In other words, the very cancer cells that had responded to the drug initially were the same ones that became resistant to the drug over time.

    The single-cell analysis also showed the researchers the specific “traffic patterns” the cells used to get around the inhibiting influence of the drug, which gave the scientists key insights about the drug combinations they could use to inhibit the mTOR protein and the proteins that provided the alternate signaling routes.

    Previous findings had suggested that drug resistance against targeted inhibitors for glioblastoma or other tumors likely occurred from one generation of cancer cells to the next — meaning that the cells could randomly develop genetic mutations that either disrupt the drug binding or counteract its effects — rather than because of individual cells’ ability to adapt. The new study was one of the first to show that cancer cells can adapt to drug treatments without genetic changes by rewiring their internal signaling circuitry.

    “By sensing this adaptation so early, we were able to anticipate and treat drug resistance,” said Heath, who is also the Elizabeth W. Gilloon Professor of Chemistry at Caltech.

    The scientists used their single cell measurements to predict three drug combinations that would stop tumor growth over the long term, as well as four drugs or drug combos that would likely have no effect. While testing all seven predictions, they found that each prediction was correct. The findings have also shown positive results in mammal models with melanoma.

    The research team also included Dr. Tim Cloughesy, a member of the Jonsson Cancer Center and professor and director of the UCLA department of neurology; Wei Wei, a first author of the study and an assistant professor of molecular and medical pharmacology at the David Geffen School of Medicine at UCLA; and Dr. Paul Mischel, a former UCLA faculty member who is now a professor at UC San Diego’s Ludwig Institute for Cancer Research.

    The research was supported by the Ben and Catherine Ivy Foundation, the National Cancer Institute and the Jean Perkins Foundation.

    See the full article here .

    Please help promote STEM in your local schools.

    STEM Icon

    Stem Education Coalition

    UC LA Campus

    For nearly 100 years, UCLA has been a pioneer, persevering through impossibility, turning the futile into the attainable.

    We doubt the critics, reject the status quo and see opportunity in dissatisfaction. Our campus, faculty and students are driven by optimism. It is not naïve; it is essential. And it has fueled every accomplishment, allowing us to redefine what’s possible, time after time.

    This can-do perspective has brought us 12 Nobel Prizes, 12 Rhodes Scholarships, more NCAA titles than any university and more Olympic medals than most nations. Our faculty and alumni helped create the Internet and pioneered reverse osmosis. And more than 100 companies have been created based on technology developed at UCLA.

     
  • richardmitnick 6:49 am on April 14, 2016 Permalink | Reply
    Tags: , Cancer,   

    From UCLA: “UCLA joins collaboration to advance cancer immunotherapy research” 

    UCLA bloc

    UCLA

    1
    UCLA’s center will be led by Dr. Antoni Ribas, who developed Keytruda, a drug that works by disabling the immune system’s “brakes,” allowing immune cells (blue) to shrink tumors (right).

    Already a national leader in cancer immunotherapy, UCLA has joined forces with five of the nation’s other leading cancer centers and The Parker Institute for Cancer Immunotherapy to maximize the potential of cancer immunotherapy research.

    The Parker Institute for Cancer Immunotherapy Center at UCLA will enable the campus’s scientists to collaborate with other leading researchers, clinicians and industry partners from around the nation, all with a common goal: to harness the power of the body’s own immune system to turn cancer into a curable disease.

    “Cancer immunotherapy is one of the most important medical advances of our time, and there is now widespread scientific consensus that the immune system is a powerful mechanism to defeat cancer,” said Dr. John Mazziotta, vice chancellor of UCLA Health Sciences and CEO of UCLA Health. “With the pioneering work being done at UCLA and the Parker Institute’s paradigm-shifting research model, we can dramatically accelerate the development of new treatments and potentially save the lives of millions of people.”

    In addition to the UCLA entity, the Parker Institute comprises new centers at UC San Francisco, New York’s Memorial Sloan Kettering Cancer Center, Stanford Medicine, the University of Pennsylvania and the University of Texas MD Anderson Cancer Center.

    Collectively, the Parker Institute for Cancer Immunotherapy unites more than 40 laboratories and more than 300 researchers from the six institutions. Each Parker Institute research center receives the funding and access to dedicated research, clinical resources and key technologies it needs to fuel discovery in cancer immunotherapy. In a unique agreement among the centers, the administration of intellectual property will be shared, granting researchers direct access to a broad set of core discoveries.

    UCLA’s effort will be led by Dr. Antoni Ribas, a professor of medicine and director of the tumor immunology program at the UCLA Jonsson Comprehensive Cancer Center.

    “This is an exciting time for cancer immunotherapy research,” Ribas said. “Now, through this initiative between UCLA and the Parker Institute, we have the potential to broaden immunotherapy’s benefits to more patients. Working with our colleagues from across the nation, we hope to be able to develop the next generation of cancer immunotherapies and test them in the clinic.”

    The Parker Institute was created through a $250 million grant from The Parker Foundation, which is the largest single contribution ever made to the field of cancer immunotherapy. The UCLA center will receive initial funding of $10 million, with an additional $10 million investment over four years.

    See the full article here .

    Please help promote STEM in your local schools.

    STEM Icon

    Stem Education Coalition

    UC LA Campus

    For nearly 100 years, UCLA has been a pioneer, persevering through impossibility, turning the futile into the attainable.

    We doubt the critics, reject the status quo and see opportunity in dissatisfaction. Our campus, faculty and students are driven by optimism. It is not naïve; it is essential. And it has fueled every accomplishment, allowing us to redefine what’s possible, time after time.

    This can-do perspective has brought us 12 Nobel Prizes, 12 Rhodes Scholarships, more NCAA titles than any university and more Olympic medals than most nations. Our faculty and alumni helped create the Internet and pioneered reverse osmosis. And more than 100 companies have been created based on technology developed at UCLA.

     
  • richardmitnick 7:18 am on April 1, 2016 Permalink | Reply
    Tags: , Cancer,   

    From UCLA: “UCLA scientists pinpoint cancer gene responsible for neuroendocrine prostate cancer” 

    UCLA bloc

    UCLA

    1
    Typical prostate cancer cells (left) and neuroendocrine prostate cancer cells. The neuroendocrine cells’ disorganized appearance reflects their more aggressive nature. UCLA Broad Stem Cell Research Center

    Scientists at the UCLA Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research have discovered that a protein produced by a cancer gene leads to the development of a deadly, late-stage form of prostate cancer called neuroendocrine prostate cancer. The discovery could be a significant step toward a more effective treatment.

    The findings, which were published in the journal Cancer Cell, are particularly important because neuroendocrine prostate cancer does not respond to standard treatments, and men who are diagnosed with the disease typically live for less than a year afterward. Up to one-quarter of those who die of prostate cancer have the neuroendocrine subtype.

    “Identifying the cellular changes that happen in cancer cells is key to the development of drugs that inhibit those changes and thereby stop the progression of the disease,” said Dr. Owen Witte, founding director of the UCLA Broad Stem Cell Research Center and the study’s lead author. Witte also is a Howard Hughes Medical Institute investigator and a member of the President’s Cancer Panel, which reports to President Barack Obama.

    With patients’ consent, the researchers obtained non-cancerous prostate basal cells — which contain prostate stem cells that can regenerate all other types of prostate cells — from men who underwent prostate surgery at the Ronald Reagan UCLA Medical Center. They then added a gene called MYCN to those cells. MYCN produces a protein called N-Myc, which is known to play a role in several types of aggressive cancer. In prostate cancer specifically, it seems to turn less aggressive prostate cancer cells into the cancer stem cells that form the aggressive neuroendocrine prostate cancer tumors.

    Next, the researchers transplanted the basal cells with the added MYCN genes into mice. Those cells with elevated N-Myc levels grew into neuroendocrine prostate cancer tumors, said Dr. John Lee, the study’s first author and a clinical instructor in the Division of Hematology Oncology at the UCLA David Geffen School of Medicine.

    2
    Dr. Owen Witte and Dr. John Lee. UCLA Broad Stem Cell Research Center

    Lee said that knowledge gave the scientists a potential new target for treating neuroendocrine prostate cancer, and they set out to begin work on a new way to attack the disease.

    Collaborating with Kevan Shokat and Dr. Clay Gustafson of UC San Francisco, the team found that an experimental drug called CD532 reduced the size of the tumors in the mice by 80 percent.

    CD532 had been developed earlier by Shokat and Gustafson for a type of childhood nervous system cancer in which N-Myc also plays a role. The drug had been shown in preclinical studies to have promise for treating that disease, but it had not previously been tested for neuroendocrine prostate cancer.

    CD532 works by changing the structure of a protein called Aurora A kinase, which stabilizes N-Myc. In the new research, CD532 effectively destabilized N-Myc and, as a result, suppressed the neuroendocrine tumors’ growth.

    Witte’s research has long sought to explain how disease develops on a cellular level. His discovery that a specific type of kinase activity, called tyrosine kinase, can play a role in certain types of leukemia became the foundation for the creation of Gleevec, the first targeted therapy for chronic myelogenous leukemia.

    “Kinase activity is known to be implicated in many types of cancers, including chronic myelogenous leukemia, which is no longer fatal for many people due to the success of Gleevec,” said Witte, who also is a member of the UCLA Jonsson Comprehensive Cancer Center and a professor of microbiology, immunology and molecular genetics at the Geffen School. “I believe we can accomplish this same result for people with neuroendocrine prostate cancer.”

    Prostate cancer is the second leading cause of cancer death in American men, after lung cancer. It is often treatable, but the chance of survival drops drastically if the tumor becomes resistant to traditional therapies and metastasizes.

    Lee said the researchers’ next steps will be to identify other drugs that may be effective for treating neuroendocrine prostate cancer.

    CD532 has only been used in preclinical tests and has not been tested in humans or approved by the U.S. Food and Drug Administration as safe and effective for use in humans.

    The research was supported by the UCLA Hal Gaba Director’s Fund for Cancer Stem Cell Research, a Tower Cancer Research Foundation Career Development Award, the National Cancer Institute, the National Institutes of Health, the Alex’s Lemonade Stand Foundation, the Department of Defense Prostate Cancer Research Program, the UCLA Jonsson Cancer Center Foundation and the UCLA Broad Stem Cell Research Center.

    The research also was supported by Prostate Cancer Foundation awards, including the Young Investigator Award, the Challenge Award and an Honorable A. David Mazzone Special Challenge Award, and by a Stand Up To Cancer–Prostate Cancer Foundation Prostate Dream Team Translational Cancer Research Grant, made possible by the generous support of the Movember Foundation. Stand Up to Cancer is a program of the Entertainment Industry Foundation administered by the American Association for Cancer Research.

    The science team:

    John K. Lee UCLA
    , John W. Phillips UCLA
    , Bryan A. Smith UCLA
    , Jung Wook Park UCLA
    , Tanya Stoyanova UCLA
    , Erin F. McCaffrey UCLA
    , Robert Baertsch UCSC
    , Artem Sokolov UCSC
    , Justin G. Meyerowitz UCSF
    , Colleen Mathis UCLA
    , Donghui Cheng UCLA
    , Joshua M. Stuart UCSC
    , Kevan M. Shokat UCSF
    , W. Clay Gustafson UCSF
    , Jiaoti Huang UCLA
    , Owen N. Witte UCLA

    See the full article here .

    Please help promote STEM in your local schools.

    STEM Icon

    Stem Education Coalition

    UC LA Campus

    For nearly 100 years, UCLA has been a pioneer, persevering through impossibility, turning the futile into the attainable.

    We doubt the critics, reject the status quo and see opportunity in dissatisfaction. Our campus, faculty and students are driven by optimism. It is not naïve; it is essential. And it has fueled every accomplishment, allowing us to redefine what’s possible, time after time.

    This can-do perspective has brought us 12 Nobel Prizes, 12 Rhodes Scholarships, more NCAA titles than any university and more Olympic medals than most nations. Our faculty and alumni helped create the Internet and pioneered reverse osmosis. And more than 100 companies have been created based on technology developed at UCLA.

     
  • richardmitnick 11:37 am on March 22, 2016 Permalink | Reply
    Tags: , , Cancer   

    From Caltech: “Nanoparticle-Based Cancer Therapies Shown to Work in Humans” 

    Caltech Logo
    Caltech

    03/21/2016
    Ker Than

    1
    Andrew Clark, an MD/PhD student in Mark Davis’s lab and the study’s first author, investigates a specimen from the study. Evidence of the nanoparticles in tumor tissue was found using fluorescence microscopy, a technique capable of detecting the chemotherapeutic drug (camptothecin) attached to the nanoparticle. In the nine patients evaluated, the nanoparticles were found only in tumor tissue and not nearby, healthy tissue. Credit: Lance Hayashida/Caltech

    A team of researchers led by Caltech scientists has shown that nanoparticles can function to target tumors while avoiding adjacent healthy tissue in human cancer patients.

    “Our work shows that this specificity, as previously demonstrated in preclinical animal studies, can in fact occur in humans,” says study leader Mark E. Davis, the Warren and Katharine Schlinger Professor of Chemical Engineering at Caltech. “The ability to target tumors is one of the primary reasons for using nanoparticles as therapeutics to treat solid tumors.”

    The findings, published online the week of March 21 in the journal Proceedings of the National Academy of Sciences, demonstrate that nanoparticle-based therapies can act as a “precision medicine” for targeting tumors while leaving healthy tissue intact.

    In the study, Davis and his colleagues examined gastric tumors from nine human patients both before and after infusion with a drug—camptothecin—that was chemically bound to nanoparticles about 30 nanometers in size.

    “Our nanoparticles are so small that if one were to increase the size to that of a soccer ball, the increase in size would be on the same order as going from a soccer ball to the planet Earth,” says Davis, who is also a member of the City of Hope Comprehensive Cancer Center in Duarte, California, where the clinical trial was conducted.

    The team found that 24 to 48 hours after the nanoparticles were administered, they had localized in the tumor tissues and released their drug cargo, and the drug had had the intended biological effects of inhibiting two proteins that are involved in the progression of the cancer. Equally important, both the nanoparticles and the drug were absent from healthy tissue adjacent to the tumors.

    The nanoparticles are designed to be flexible delivery vehicles. “We can attach different drugs to the nanoparticles, and by changing the chemistry of the bond linking the drug to the nanoparticle, we can alter the release rate of the drug to be faster or slower,” says Andrew Clark, a graduate student in Davis’s lab and the study’s first author.

    Davis says his team’s findings suggest that a phenomenon known as the enhanced permeability and retention (EPR) effect is at work in humans. In the EPR effect, abnormal blood vessels that are “leakier” than normal blood vessels in healthy tissue allow nanoparticles to preferentially concentrate in tumors. Until now, the existence of the EPR effect has been conclusively proven only in animal models of human cancers.

    “Our results don’t prove the EPR effect in humans, but they are completely consistent with it,” Davis says.

    The findings could also help pave the way toward more effective cancer drug cocktails that can be tailored to fight specific cancers and that leave patients with fewer side effects.

    “Right now, if a doctor wants to use multiple drugs to treat a cancer, they often can’t do it because the cumulative toxic effects of the drugs would not be tolerated by the patient,” Davis says. “With targeted nanoparticles, you have far fewer side effects, so it is anticipated that a drug combination can be selected based on the biology and medicine rather than the limitations of the drugs.”

    These nanoparticles are currently being tested in a number of phase-II clinical trials. (Information about trials of the nanoparticles, denoted CRLX101, is available at http://www.clinicaltrials.gov).

    In addition to Davis and Clark, other coauthors on the study, entitled “CRLX101 nanoparticles localize in human tumors and not in adjacent, nonneoplastic tissue after intravenous dosing,” include Devin Wiley (MS ’11, PhD ’13) and Jonathan Zuckerman (PhD ’12); Paul Webster of the Oak Crest Institute of Science; Joseph Chao and James Lin at City of Hope; and Yun Yen of Taipei Medical University, who was at City of Hope and a visitor in the Davis lab at the initiation of the clinical trial. The research was supported by grants from the National Cancer Institute and the National Institutes of Health and by Cerulean Pharma Inc. Davis is a consultant to and holds stock in Cerulean Pharma Inc.

    See the full article here .

    Please help promote STEM in your local schools.

    STEM Icon

    Stem Education Coalition

    The California Institute of Technology (commonly referred to as Caltech) is a private research university located in Pasadena, California, United States. Caltech has six academic divisions with strong emphases on science and engineering. Its 124-acre (50 ha) primary campus is located approximately 11 mi (18 km) northeast of downtown Los Angeles. “The mission of the California Institute of Technology is to expand human knowledge and benefit society through research integrated with education. We investigate the most challenging, fundamental problems in science and technology in a singularly collegial, interdisciplinary atmosphere, while educating outstanding students to become creative members of society.”
    Caltech buildings

     
  • richardmitnick 11:11 am on March 22, 2016 Permalink | Reply
    Tags: , Cancer,   

    From MedicalXpress: “FOXA1 found to control specificity of cancer cells” 

    Medicalxpress bloc

    MedicalXpress

    March 21, 2016
    Bob Yirka

    1
    Electron microscopic image of a single human lymphocyte. Credit: Dr. Triche, National Cancer Institute

    A team of researchers with the Mayo Clinic has learned more about how a transcription factor known as FOXA1 forms cancer-specific genomic identifiers and how it regulates gene expression differently among four very different types of human cancer cell lines. In their paper published in the journal Science Advances, the team describes how they used gene editing techniques and other tools to learn more about the unique binding process that allows the protein to regulate gene expression in the different types of cancers.

    Scientists know that cancer doesn’t grow in isolation, tumors, like other parts of the body are made of cells which depend on the same biological processes to regulate organogenesis as other tissues or organs. One of those processes is transcriptional regulation, where cells regulate the conversion of DNA sequences to RNA. In this new effort, the researchers looked at the protein coding gene FOXA1, which has been associated with several types of human cancers. More specifically, they looked into how just one transcription factor is able to form cancer-specific genomic changes to different types of cells, because it is important when trying to understand how tumors grow and because to date, it is still not very well understood.

    The researchers started with a type of sequencing technology that allows for processing large numbers of genomes, which allowed them to see how FOXA1 targets genes in two different kinds of breast cancer cells as well as liver and prostate cancer cells—and that allowed them to see a previously unknown feature of the protein; tailored targeting and binding to DNA. The team then used the CRISPR- Cas9 genome editing technique to look deeper and found that cell-specific FOXA1 regulation was due to unique binding, genetic variations and/or possible non-genetic regulation, which added more evidence of FOXA1 controlling the process by which specific types of cancer cells develop.

    After analyzing their work, the team developed a hypothesis to describe how they believe the process works, describing it as a progression that looks rather like what happens when a flower blooms. They suggest that the ‘blooming’ of certain transcription factors may be managed by the uniqueness of its genetic variations, its unique binding abilities and likely some other possible factors which may include other regulators and/or chromatin remodeling. The net result is more information regarding the mechanism behind the growth of cancer cells, which adds to an ever growing body of data that may one day reveal a means for controlling such growth and thus preventing cancer from causing harm.

    More information: G. Zhang et al. FOXA1 defines cancer cell specificity, Science Advances (2016). DOI: 10.1126/sciadv.1501473

    See the full article here .

    Please help promote STEM in your local schools.

    STEM Icon

    Stem Education Coalition

    Medical Xpress is a web-based medical and health news service that is part of the renowned Science X network. Medical Xpress features the most comprehensive coverage in medical research and health news in the fields of neuroscience, cardiology, cancer, HIV/AIDS, psychology, psychiatry, dentistry, genetics, diseases and conditions, medications and more.

     
  • richardmitnick 5:14 pm on March 21, 2016 Permalink | Reply
    Tags: , Cancer, ,   

    From MedicalXpress: ” ‘Silencer molecules’ switch off cancer’s ability to spread around body” 

    Medicalxpress bloc

    MedicalXpress

    March 21, 2016
    No writer credit found

    1

    Scientists have revealed that a key molecule in breast and lung cancer cells can help switch off the cancers’ ability to spread around the body.

    The findings by researchers at Imperial College London, published in the journal EMBO Reports, may help scientists develop treatments that prevent cancer travelling around the body—or produce some kind of test that allows doctors to gauge how likely a cancer is to spread.

    During tumour growth, cancer cells can break off and travel in the bloodstream or lymph system to other parts of the body, in a process called metastasis.

    Patients whose cancers spread tend to have a worse prognosis, explains Professor Justin Stebbing, senior author of the study from the Department of Surgery and Cancer at Imperial: “The ability of a cancer to spread around the body has a large impact on a patient’s survival. However, at the moment we are still in the dark about why some cancers spread around the body—while others stay in one place. This study has given important insights into this process.”

    The researchers were looking at breast and lung cancer cells and they found that a protein called MARK4 enables the cells to break free and move around to other parts of the body, such as the brain and liver. Although scientist are still unsure how it does this, one theory is it affects the cell’s internal scaffolding, enabling it to move more easily around the body.

    The team found that a molecule called miR-515-5p helps to silence, or switch off, the gene that produces MARK4.

    In the study, the team used human breast cancer and lung cancer cells to show that the miR-515-5p molecule silences the gene MARK4. They then confirmed this in mouse models, which showed that increasing the amount of miR-515-5p prevents the spread of cancer cells. The findings also revealed that the silencer molecule was found in lower levels in human tumours that had spread around the body.

    The team then also established that patients with breast and lung cancers whose tumours had low amounts of these silencer molecules—or high amounts of MARK4—had lower survival rates.

    Researchers are now investigating whether either the MARK4 gene or the silencer molecule could be targeted with drugs. They are also investigating whether these molecules could be used to develop a test to indicate whether a patient’s cancer is likely to spread.

    Professor Stebbing said: “In our work we have shown that this silencer molecule is important in the spread of cancer. This is very early stage research, so we now need more studies to find out more about this molecule, and if it is present in other types of cancer.”

    Dr Olivier Pardo, lead author of the paper, also from the Department of Surgery and Cancer at Imperial, added: “Our work also identified that MARK4 enables breast and lung cancer cells to both divide and invade other parts of the body. These findings could have profound implications for treating breast and lung cancers, two of the biggest cancer killers worldwide.”

    More information: O. E. Pardo et al. miR-515-5p controls cancer cell migration through MARK4 regulation, EMBO reports (2016). DOI: 10.15252/embr.201540970

    See the full article here .

    Please help promote STEM in your local schools.

    STEM Icon

    Stem Education Coalition

    Medical Xpress is a web-based medical and health news service that is part of the renowned Science X network. Medical Xpress features the most comprehensive coverage in medical research and health news in the fields of neuroscience, cardiology, cancer, HIV/AIDS, psychology, psychiatry, dentistry, genetics, diseases and conditions, medications and more.

     
c
Compose new post
j
Next post/Next comment
k
Previous post/Previous comment
r
Reply
e
Edit
o
Show/Hide comments
t
Go to top
l
Go to login
h
Show/Hide help
shift + esc
Cancel
Follow

Get every new post delivered to your Inbox.

Join 551 other followers

%d bloggers like this: