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  • richardmitnick 3:35 pm on September 2, 2015 Permalink | Reply
    Tags: , Cancer,   

    From NOVA: “Venom of Aggressive Brazilian Wasp Rips Holes in Cancer Cells” 



    Polybia paulista

    Until a decade ago, Polybia paulista wasn’t well known to anyone other than entomologists and the hapless people it stung in its native Brazil. But then, a number of research groups discovered a series of remarkable qualities all concentrated in the aggressive wasp’s venom.

    One compound in particular has stood out for its antimicrobial and anti-cancer properties. Polybia-MP1, a peptide, or a string of amino acids, is different from most antibacterial peptides in that it’s only toxic to bacteria and not red blood cells. MP1 punches through bacteria’s cell membranes, causing them to die a leaky death. Scientists had also discovered that MP1 was also good at inhibiting spreading bladder and prostate cancer cells and could kill leukemia cells, but they didn’t know why it was so toxic only to tumor cells.

    Well, now they think they have an idea. How MP1 kills cancer cells turns out to be very similar to how it kills bacteria cells—by causing them to leak to death. MP1 targets two lipids— phosphatidylserine, or PS, and phosphatidylethanolamine, or PE—that cancer cells have adorned on the outside of their membranes. Here’s Kiona Smith-Strickland, writing for Discover:

    MP1’s destruction of a cancer cell, researchers say, has two stages. First, MP1 bonds to the outer surface of the cell, and then it opens holes or pores in the membrane big enough to let the cell’s contents leak out. PS is crucial for the first part: seven times more MP1 molecules bound to membranes with PS in their outer layer. And PE is crucial for the second: Once the MP1 molecules worked their way into the membrane, they opened pores twenty to thirty times larger than in membranes without PE.

    Even better, healthy cells have neither PS nor PE on the outside of their membranes. Rather, they keep them on the inside, a key difference from cancer cells that would shield them from the damaging effects of MP1. In other words, MP1 could make an ideal chemotherapy.

    See the full article here.

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    NOVA is the highest rated science series on television and the most watched documentary series on public television. It is also one of television’s most acclaimed series, having won every major television award, most of them many times over.

  • richardmitnick 2:38 pm on August 31, 2015 Permalink | Reply
    Tags: , Cancer, Help Conquer Cancer project,   

    From WCG: “Analyzing crystals to help fight cancer” 

    New WCG Logo

    28 Aug 2015
    Help Conquer Cancer research team

    Behind-the-scenes work continues on the Help Conquer Cancer project – the team is analyzing millions of protein crystallization images processed by World Community Grid volunteers, with the hope of finding patterns that will help researchers build better cancer screening tools.

    Dear World Community Grid volunteers:

    We continue to analyze the millions of protein-crystallization images that you processed as part of Help Conquer Cancer (HCC), with the end goal of gaining insight into the crystallization process. In turn, this will enable us to crystalize cancer and other disease-related proteins, determine their structure, function, and design drugs accordingly. We aim to identify non-trivial, interesting and ultimately useful patterns in this large and valuable data set.

    We strive to integrate more detailed data we have received from Hauptman Woodward Institute which will allow us to interpret patterns we are identifying and linking properties of proteins, conditions, and temporal data to specific images that were processed on World Community Grid. Work is ongoing, albeit more slowly at present, as the Post Doctoral Fellow working on the integration and data mining had to take a leave of absence to expand her teaching skills. Christian continues to dedicate some of his time to the HCC project, but also had to expand on the analysis and streamline infrastructure to support our Mapping Cancer Markers project.

    We have been working on some novel analysis angles with a visiting student from Denmark, and a new student is expected to start working on the project in the Fall 2015. We therefore expect to be able to give you more detailed results in the next HCC update, which we will provide in a few months.

    See more detail in the original article.

    See the full article here.

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    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.


    “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-
    Outsmart Ebola together

    Outsmart Ebola Together

    Mapping Cancer Markers

    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


    Computing for Sustainable Water

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

    IBM – Smarter Planet

  • richardmitnick 1:12 pm on August 29, 2015 Permalink | Reply
    Tags: , Cancer,   

    From UBC: “Breakthrough discoveries change how we understand breast cancer” 

    U British Columbia bloc

    University of British Columbia

    No Writer Credit

    No image credit

    Through a series of major breakthrough studies, scientists at UBC and the BC Cancer Agency have transformed our understanding of breast cancer and set the stage for the development of new treatments.

    It began with a landmark discovery in 2009.

    By decoding—for the first time in history—the three billion letters in the DNA sequence of a patient’s metastatic lobular breast cancer and following its evolution over nine years, Dr. Samuel Aparicio, Dr. Marco Marra and Dr. Sohrab Shah were able to show how this complex cancer mutates and spreads.

    Aparicio is a Professor in the Department of Pathology and Laboratory Medicine at UBC and heads the BC Cancer Agency’s Department of Molecular Oncology; Marra directs the Michael Smith Genome Sciences Centre and the Department of Medical Genetics at UBC; and Shah is an Associate Professor in the Department of Pathology and Laboratory Medicine at UBC, a Scientist at the BC Cancer Agency, and Canada Research Chair in Computational Cancer Genomics.

    The research team they led found that of the 32 mutations in the metastatic tumour, only five could have been present in all the cells of the original tumour, thereby identifying them as the suspected cause of the disease getting started in the first place.

    The internationally significant findings were published in the prestigious journal Nature.

    “This is a watershed event in our ability to understand the causes of breast cancer and to develop personalized medicines for our patients,” declared Aparicio at the time.

    In 2012, international research led by Aparicio at the BC Cancer Agency and Dr. Carlos Caldas at the Cancer Research UK Cambridge Institute was able to classify breast cancer into ten subtypes. They then grouped these subtypes by common genetic features, which correlate with survival, to suggest how treatments could be tailored to treat women with better defined types of breast cancer.

    This discovery followed on the heels of Aparicio, Shah and Marra leading the decoding of the most deadly triple-negative breast cancer. This research similarly discovered new genes that had never before been linked to the disease and showed that breast cancer is an umbrella term for what is really a number of unique diseases.

    Aparicio and Shah have since led further research to understand and predict how these complex cancers evolve over time.

    The two researchers used Shah’s statistical modelling software, PyClone, to analyze the billions of pieces of genetic data gathered from the tumour samples. Their findings, published in Nature in 2014, provided a map for how certain breast cancers evolve to become drug resistant over time.

    “By pinpointing which individual cancer cells are the ‘resilient’ ones that are most likely to have an impact on patient survival,” says Shah, “We are paving the way for drug development and treatment practices that will stop these cellular superbugs from taking over.”

    “Because of this research we have a way to identify the cancer ‘super-cells’ and stay one step ahead of disease progression by tailoring effective treatments to individual patients,” adds Aparicio.

    It’s a radical shift in the way we understand cancer—one that is of vital importance to both the global cancer research community and to future drug studies.

    See the full article here.

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    U British Columbia Campus

    The University of British Columbia is a global centre for research and teaching, consistently ranked among the 40 best universities in the world. Since 1915, UBC’s West Coast spirit has embraced innovation and challenged the status quo. Its entrepreneurial perspective encourages students, staff and faculty to challenge convention, lead discovery and explore new ways of learning. At UBC, bold thinking is given a place to develop into ideas that can change the world.

  • richardmitnick 8:19 pm on August 27, 2015 Permalink | Reply
    Tags: , Cancer,   

    From Salk: ” New drug squashes cancer’s last-ditch efforts to survive” 

    Salk Institute bloc

    Salk Institute for Biological Studies

    The Salk Institute and Sanford Burnham Prebys Medical Discovery Institute created a compound that stops a cellular recycling process

    Cell recycling (shown in green) is elevated in lung cancer cells treated with an established cancer drug. Recycling is suppressed upon co-treatment with a newly discovered enzyme inhibitor.
    Image: Courtesy of the Salk Institute for Biological Studies

    Salk Institute and Sanford Burnham Prebys Medical Discovery Institute (SBP) scientists have developed a drug that prevents this process from starting in cancer cells. Published June 25, 2015 in Molecular Cell, the new study identifies a small molecule drug that specifically blocked the first step of autophagy, effectively cutting off the recycled nutrients that cancer cells need to live.

    “The finding opens the door to a new way to attack cancer,” says Reuben Shaw, a senior author of the paper, professor in the Molecular and Cell Biology Laboratory at the Salk Institute and a Howard Hughes Medical Institute Early Career Scientist. “The inhibitor will probably find the greatest utility in combination with targeted therapies.”

    Besides cancer, defects in autophagy have been linked with infectious diseases, neurodegeneration and heart problems. In a 2011 study in the journal Science, Shaw and his team discovered how cells starved of nutrients activate the key molecule that kicks off autophagy, an enzyme called ULK1.

    Reasoning that inhibiting ULK1 might snuff out some types of cancer by stifling a main energy supply that comes from the recycling process, Shaw’s group and others wanted to find a drug that would inhibit the enzyme. Only a fraction of such inhibitors that show promise in a test tube end up working well in living cells. Shaw’s group spent more than a year studying how ULK1 works and developing new strategies for screening its function in cells.

    A key breakthrough came when Shaw met the paper’s other senior author, Nicholas Cosford, a professor in the NCI-Designated Cancer Center at SBP. Cosford had been investigating ULK1 using medicinal chemistry and chemical biology, and had identified some promising lead compounds using rational design. The two labs combined efforts to screen hundreds of potential molecules for ULK1 inhibition, narrowing the list down to a few dozen, and eventually one.

    “The key to success for this project came when we combined Reuben’s deep understanding of the fundamental biology of autophagy with our chemical expertise,” says Cosford. “This allowed us to find a drug that targeted ULK1 not just in a test tube but also in tumor cells. Another challenge was finding molecules that selectively targeted the ULK1 enzyme without affecting healthy cells. Our work provides the basis for a novel drug that will treat resistant cancer by cutting off a main tumor cell survival process.”

    The result was a highly selective drug they named SBI-0206965, which successfully killed a number of cancer cell types, including human and mouse lung cancer cells and human brain cancer cells, some of which were previously shown to be particularly reliant on cellular recycling.

    Interestingly, some cancer drugs (such as mTOR inhibitors) further activate cell recycling by shutting off the ability of those cells to take up nutrients, making them more reliant on recycling to provide all the building blocks cells need to stay alive. Rapamycin, for example, works by shutting down cell growth and division. In response, the cells launch into recycling mode by turning on ULK1, which may be one reason why, rather than dying, some cancer cells seem to go into a dormant state and return–often more drug resistant–after treatment stops.

    Matthew Chun, Nicholas Cosford and Reuben Shaw. Image: Courtesy of the Salk Institute for Biological Studies

    “Inhibiting ULK1 would eliminate this last-ditch survival mechanism in the cancer cells and could make existing anti-cancer treatments much more effective,” says Matthew Chun, one of the study’s lead authors and a postdoctoral fellow in the Shaw lab at Salk.

    Indeed, combining SBI-0206965 with mTOR inhibitors made it more effective, killing two to three times as many lung cancer cells as SBI-0206965 alone or the mTOR inhibitors alone.

    Drugging the autophagy pathway to combat cancer has been tried before, but the only drugs that currently block cell recycling work by targeting the cell organelle known as the lysosome, which functions at the final stage of autophagy. Although these lysosomal therapies are being tested in early-stage clinical trials, they inhibit other lysosomal functions beyond autophagy, and therefore may have additional side effects.

    Comparing equivalent concentrations of the lysosomal drug chloroquine with SBI-0206965, in combination mTOR inhibitors, the scientists found that SBI-0206965 was better than chloroquine at killing cancer cells.

    The group is now testing the drug in mouse models of cancer. “An important next step will be testing this drug in other types of cancer and with other therapeutic combinations,” says Shaw, who is deputy director of Salk’s NCI-Designated Cancer Center. “In the meantime, this discovery gives researchers an exciting new toolbox for the inhibition and measurement of cell recycling.”

    Other authors on the study include co-lead author Daniel Egan of Salk’s Molecular and Cell Biology Laboratory; Mitchell Vamos, Haixia Zou, Juan Rong, Dhanya Raveendra-Panickar, Douglas Sheffler, and Peter Teriete of the Cell Death and Survival Networks Research Program in the NCI-Designated Cancer Center at SBP; Chad Miller, Hua Jane Lou, and Benjamin Turk of the Department of Pharmacology in Yale University School of Medicine; John Asara of the Division of Signal Transduction in Beth Israel Deaconess Medical Center and the Department of Medicine in Harvard Medical School; and Chih-Cheng Yang of SBP’s Functional Genomics Core.

    The research was supported by National Institutes of Health, the Department of Defense, and the Leona M. and Harry B. Helmsley Charitable Trust.

    See the full article here.

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    Salk Institute Campus

    Every cure has a starting point. Like Dr. Jonas Salk when he conquered polio, Salk scientists are dedicated to innovative biological research. Exploring the molecular basis of diseases makes curing them more likely. In an outstanding and unique environment we gather the foremost scientific minds in the world and give them the freedom to work collaboratively and think creatively. For over 50 years this wide-ranging scientific inquiry has yielded life-changing discoveries impacting human health. We are home to Nobel Laureates and members of the National Academy of Sciences who train and mentor the next generation of international scientists. We lead biological research. We prize discovery. Salk is where cures begin.

  • richardmitnick 8:06 pm on August 27, 2015 Permalink | Reply
    Tags: , Cancer,   

    From Yale: “Research in the news: Study reveals new way to ‘rewire’ immune cells to slow tumor growth” 

    Yale University bloc

    Yale University

    August 27, 2015
    Ziba Kashef

    (Image via Shutterstock)

    Inside a tumor, immune cells and cancer cells battle for survival. The advantage may go to the cells that metabolize the most glucose, say Yale researchers who have identified a new way to boost immune response by metabolically “rewiring” immune cells.

    Their research, published Aug. 27 online in Cell, may provide a novel approach to cancer immunotherapy.

    Researchers have long known that specific immune cells known as T cells infiltrate tumors. But tumor-infiltrating T cells fail to destroy cancer cells, in part, because inside the tumor they are deprived of glucose, a nutrient essential to T cell function. The research team, led by professor of immunobiology Susan Kaech and postdoctoral fellow Ping-Chih Ho, theorized that metabolic reprogramming of T cells could enhance their anti-tumor response.

    When cells eat glucose, they convert it into a metabolite called phosphoenolpyruvate (PEP). Using biochemical analyses, the researchers identified a new role for PEP in fine-tuning the anti-tumor response of T cells. They genetically reprogrammed the T cells to increase PEP production, restoring cell function and slowing tumor growth.

    The research reveals a potential new form of cancer immunotherapy. “Knowing how the metabolic state of T cells is affected in tumors, we may find new ways of altering their metabolism to make them more efficiently kill tumor cells,” says Kaech. These types of approaches could be directly applied to clinical trials using adoptive T cell therapy, she notes.

    The study results may also apply to conditions other than cancer. “Understanding how immune cell metabolism affects their function could lead to novel approaches to adjust immune responses in a variety of diseases,” says Ho.

    See the full article here.

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    Yale University Campus

    Yale University comprises three major academic components: Yale College (the undergraduate program), the Graduate School of Arts and Sciences, and the professional schools. In addition, Yale encompasses a wide array of centers and programs, libraries, museums, and administrative support offices. Approximately 11,250 students attend Yale.

  • richardmitnick 7:08 pm on August 24, 2015 Permalink | Reply
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    From Yale: “Research in the news: Yale scientists develop novel technique for kidney research” 

    Yale University bloc

    Yale University

    August 24, 2015

    Ziba Kashef


    One in four patients treated with the widely used anti-cancer drug cisplatin develop chronic kidney disease. To better understand how the treatment leads to kidney damage, and possibly prevent it, a team of researchers at Yale School of Medicine developed a new 3D-imaging technique to peer deep into these vital organs.

    Their study was published online Aug. 24 in the Journal of the American Society of Nephrology.

    New imaging technique shows internal structures of normal kidney (a) versus damage in response to anti-cancer drug (b and c).

    Using a mouse model, the Yale team, led by professor of nephrology Dr. Robert Safirstein, administered doses of cisplatin two weeks apart. To examine the effect of the drug on kidneys, the researchers combined a powerful imaging technique, multiphoton microscopy, with a clearing solution that produced high-resolution 3D images of the organ.

    The novel strategy provided an unusually deep view of the kidney’s internal structures. “Before this technique, you could only look at the very superficial surface, so you really couldn’t examine the entire kidney,” said Safirstein.

    To their surprise, the researchers uncovered evidence that the kidneys failed and developed damaged tubules (key structures that the kidney uses to transport fluids) before damage was detectable through more traditional methods.

    The findings could shift the direction of kidney research. “It changes the focus of research in kidney disease to find out how lesions form,” Safirstein noted. The imaging technique could also inform the study of diabetes and other conditions. “We think this is going to be applicable in a wide variety of diseases,” he noted.

    Additional authors include Dr. Richard Torres, Heino Velazquez, Dr. John J. Chang, Michael J. Levene, Dr. Gilbert Moeckel, and Dr. Gary V. Desir.

    See the full article here.

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    Yale University Campus

    Yale University comprises three major academic components: Yale College (the undergraduate program), the Graduate School of Arts and Sciences, and the professional schools. In addition, Yale encompasses a wide array of centers and programs, libraries, museums, and administrative support offices. Approximately 11,250 students attend Yale.

  • richardmitnick 6:08 pm on August 24, 2015 Permalink | Reply
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    From Rockefeller: “Promising class of new cancer drugs cause memory loss in mice” 

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    Rockefeller University

    August 24, 2015
    Eva Kiesler | 212-327-7963

    A striking brain presence: Neurons throughout the mouse brain produce Brd4, a protein targeted by some new cancer drugs. In this cross-section of a mouse brain, Brd4-producing cells are stained red but appear purple against a blue stain that labels all cells.

    Cancer researchers are constantly in search of more-effective and less-toxic approaches to stopping the disease, and have recently launched clinical trials testing a new class of drugs called BET inhibitors. These therapies act on a group of proteins that help regulate the expression of many genes, some of which play a role in cancer.

    New findings from The Rockefeller University suggest that the original version of BET inhibitors causes molecular changes in mouse neurons, and can lead to memory loss in mice that receive it. Published in Nature Neuroscience on August 24, the study was led by C. David Allis, Joy and Jack Fishman Professor in the Laboratory of Chromatin Biology and Epigenetics, in collaboration with Robert B. Darnell, Robert and Harriet Heilbrunn Professor and head of the Laboratory of Molecular Neuro-Oncology.

    The findings will likely fuel more research into the brain effects of BET inhibitors, and could lead to the development of safer drugs that reduce the risk of potential side effects such as memory loss.

    First author Erica Korb, a postdoctoral fellow in Allis’s lab, says the compound they tested in the study has the ability to cross into the brain from the bloodstream. However, this may not be the case for other drug variants tested in patients. Several companies are testing the inhibitors using unique formulations that they’ve optimized in proprietary ways — for example, by adding chemical groups to make a compound more targeted or effective — which might make it more difficult for the drug to cross the blood-brain barrier.

    Many patients with hard-to-treat cancers have already received these experimental drugs. The Rockefeller scientists say their findings suggests more research is needed to determine whether the therapies can enter the brain, since that could potentially cause some unwanted side effects. “We found that if a drug blocks a BET protein throughout the body, and that drug can get into the brain, you could very well produce neurological side effects,” says Korb.

    Allis, Korb, and their colleagues decided to test BET inhibitors in the brain. BET proteins help regulate the process of transcribing genes into proteins, a key step in cell division. Since neurons divide less frequently than other cell types, scientists hadn’t given much consideration to the role of BET proteins in the brain, says Korb.

    During the study, the researchers used a compound that was designed to thwart the activity of a specific BET protein, called Brd4. They used the original version of the drug, called Jq1, says Korb, which they knew could cross the blood-brain barrier.

    The researchers added the drug to mouse neurons grown in the laboratory, then stimulated the cells in a way that mimicked the process of memory formation. Normally, when neurons receive this type of signal, they begin transcribing genes into proteins, resulting in the formation of new memories — a process that is partly regulated by Brd4. “To turn a recent experience into a long-term memory, you need to have gene transcription in response to these extracellular signals,” says Korb.

    Indeed, when the researchers stimulated mouse neurons with signals that mimicked those they would normally receive in the brain, they saw massive changes in gene transcription. But when they performed this experiment after adding Jq1, they saw much less activity. “After administering a Brd4 inhibitor, we no longer saw those changes in transcription after stimuli,” says Korb.

    To test how the drug affected mice’s memories, researchers placed the animals in a box with two objects they’ve never seen before, such as pieces of lego or tiny figurines. Mice typically explore anything unfamiliar, climbing and sniffing around it. After a few minutes, the researchers took the mice out of the box. One day later, they put them back in, this time with one of the objects from the day before and another, unfamiliar one.

    Mice that received the placebo drug were much more interested in the new object, presumably because the one from the day before was familiar. But mice treated with Jq1 were equally interested in both objects, suggesting they didn’t remember the previous day’s experience.

    Next, the researchers took their findings one step further. If Jq1 reduces molecular activity in the brain, they asked, could it help in conditions marked by too much brain activity, such as epilepsy?

    Brd4 regulates a receptor protein present at the synapse, a structure where two neurons connect and transmit signals. When the researchers administered the Brd4 inhibitor, they saw decreased levels of that receptor, which likely results in neurons firing less frequently. Next, they gave the drug to mice for a week, then added a chemical that induces seizures.

    The experiment showed that mice that received Jq1 had a much lower rate of seizures than those given a placebo drug. “In the case of the epileptic brain, when there’s too much activity and neurons talking to each other, this drug could be potentially be beneficial,” says Korb. “Extending the use of these drugs into non-cancer diseases, including neurological disorders, is a largely unexplored area with much potential,” Allis adds.

    See the full article here.

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    The Rockefeller University is a world-renowned center for research and graduate education in the biomedical sciences, chemistry, bioinformatics and physics. The university’s 76 laboratories conduct both clinical and basic research and study a diverse range of biological and biomedical problems with the mission of improving the understanding of life for the benefit of humanity.

    Founded in 1901 by John D. Rockefeller, the Rockefeller Institute for Medical Research was the country’s first institution devoted exclusively to biomedical research. The Rockefeller University Hospital was founded in 1910 as the first hospital devoted exclusively to clinical research. In the 1950s, the institute expanded its mission to include graduate education and began training new generations of scientists to become research leaders around the world. In 1965, it was renamed The Rockefeller University.

  • richardmitnick 5:38 pm on August 24, 2015 Permalink | Reply
    Tags: , Cancer,   

    From Weizmann: “Opposite Effects” 

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    Weizmann Institute of Science

    No Writer Credit

    Cultured colorectal cancer cells. Top: Cells that have become resistant to certain forms of chemotherapy and continue to thrive. Bottom: The same cells, which have had the LIP gene inserted and are then treated with chemotherapy drugs

    Only the strongest survive. This is not always a good thing: Some very small, but very strong and very deadly survivors – cancer cells – may persevere after chemotherapy. In research that recently appeared in the Journal of the National Cancer Institute, Prof. Menachem Rubinstein of the Weizmann Institute’s Molecular Genetics Department suggests that cancer cells that have developed resistance to chemotherapy may have an Achilles’ heel that can be exploited to weaken them so they can be killed.

    Following chemotherapy – a combination of drugs that kills tumor cells – the cancer sometimes comes back; and it may be stronger and more resistant to treatment than before. The pharmaceutical industry was focused for quite a while on proteins on the cells’ outer wall that act as “pumps” for expelling the drugs from the cell. But blocking these pumps did not solve the problem of drug resistance.

    Rubinstein and his research group decided to take a step back and have another look at what makes a cancer cell resistant to chemotherapy. “We figured that if blocking the pumps did not solve the problem, there must be some other mechanism of resistance,” he says. The research conducted in his lab – led by visiting scientist Prof. Chiara Riganti from the University of Torino, together with Sara Barak – showed that a protein called CEBP can appear in cancer cells in two different forms. These two forms, called LIP and LAP, have opposite effects on the cancer cell.

    LAP, the long form of the protein, is a functional protein, while LIP, the short version, binds in the same way but does not perform any work. Earlier research in Rubinstein’s group had shown that LAP works to avert cell death when the cancer cells are exposed to stress, while LIP, because it binds to the same locations as LAP but does not carry through, actually expedites cancer cell death.

    In the present study, Rubinstein and Riganti discovered, to their surprise, that chemotherapy-resistant cells from many kinds of cancer do not contain any LIP at all. When they inserted the genes for LIP into these cells, the cells began to respond well to the chemotherapy drugs.

    Once again Rubinstein took a step back to ask: Why is there no LIP in these chemotherapy-resistant cells? Further investigation revealed that these cells actually do produce the short, LIP, form of the protein. It is just that the cellular degradation machinery takes LIP apart as soon as it is produced. The solution to the problem appeared to be simple: The scientists demonstrated that existing drugs that have been approved for other uses inhibited the process by which LIP is degraded.

    Experiments with tumor cells cultured in the lab have yielded positive results. Much more research is required before we will know if the drugs are effective against cancers in the human body, but the scientists envision them being used in combination with current chemotherapy, weakening the cells’ resistance so that the chemotherapy can eliminate them.

    Prof. Menachem Rubinstein’s research is supported by the Jeanne and Joseph Nissim Foundation for Life Sciences Research; the Bernard and Audrey Jaffe Foundation; and the Adelis Foundation. Prof. Rubinstein is the incumbent of the Maurice and Edna Weiss Professorial Chair of Cytokines Research.

    See the full article here.

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    Weizmann Institute Campus

    The Weizmann Institute of Science is one of the world’s leading multidisciplinary research institutions. Hundreds of scientists, laboratory technicians and research students working on its lushly landscaped campus embark daily on fascinating journeys into the unknown, seeking to improve our understanding of nature and our place within it.

    Guiding these scientists is the spirit of inquiry so characteristic of the human race. It is this spirit that propelled humans upward along the evolutionary ladder, helping them reach their utmost heights. It prompted humankind to pursue agriculture, learn to build lodgings, invent writing, harness electricity to power emerging technologies, observe distant galaxies, design drugs to combat various diseases, develop new materials and decipher the genetic code embedded in all the plants and animals on Earth.

    The quest to maintain this increasing momentum compels Weizmann Institute scientists to seek out places that have not yet been reached by the human mind. What awaits us in these places? No one has the answer to this question. But one thing is certain – the journey fired by curiosity will lead onward to a better future.

  • richardmitnick 3:04 pm on August 24, 2015 Permalink | Reply
    Tags: , , Cancer, Immunotherapy   

    From AAAS: “The cancer therapy breakthrough that gives President Carter hope” 



    Jimmy Carter in conversation at the LBJ Library on 15 February 2011. U.S. National Archives

    21 August 2015
    Jennifer Couzin-Franke

    Former U.S. President Jimmy Carter appeared relaxed and even made the occasional joke when he publicly announced yesterday that he has melanoma that has spread to his liver and brain. The 90-year-old expressed hope that he’d benefit, as many are these days, from cutting-edge therapies that help the immune system destroy cancer cells. (These treatments topped Science’s Breakthroughs of the Year in 2013.) Melanoma, in some patients, was among the first cancers to succumb to one of these immunotherapies, and the specific treatment Carter is taking has many oncologists excited: It’s a monoclonal antibody called pembrolizumab and sold under the brand name Keytruda. Approved in the United States a year ago for advanced melanoma, pembrolizumab belongs to a hot class of drugs called PD-1 inhibitors. By blocking the PD-1 protein, the therapy allows the body to make T cells that can chase after a cancer.

    Still, researchers have a lot to learn about pembrolizumab and other PD-1 therapies in development. Keytruda is also extremely expensive, at about $150,000 a year. In clinical trials, PD-1 blockers generally work in less than half the participants. Research published earlier this year suggested PD-1 inhibitors may work best on tumors with lots of mutations, and a small clinical trial of pembrolizumab backed this up. It found that people with advanced cancer were far more likely to respond if they had so-called mismatch repair mutations in their tumors. This could also help explain why, so far, PD-1 inhibitors have produced the best outcomes in people with lung cancer and melanoma—both are often mutation-heavy tumors.

    What all this means for individual cancer patients such as Carter is still uncertain. “I’ve had a wonderful life,” he said in a televised news conference from the Carter Center in Atlanta, smiling broadly. “I’ll be prepared for anything that comes.”

    See the full article here.

    The American Association for the Advancement of Science is an international non-profit organization dedicated to advancing science for the benefit of all people.

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  • richardmitnick 1:59 pm on August 21, 2015 Permalink | Reply
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    From Rice: “Imaging software could speed breast cancer diagnosis” 

    Rice U bloc

    Rice University

    August 21, 2015
    Jade Boyd

    Technology could improve access to diagnostic services in developing countries

    Rebecca Richards-Kortum

    New software developed by Rice University bioengineers could speed up the diagnosis of breast cancer with 90 percent accuracy and without the need for a specialist, according to research published this week in the open-access journal Breast Cancer Research.

    Researchers said the software could improve breast cancer management, particularly in developing countries where pathologists are not routinely available.

    “To evaluate fresh breast tissue at the point of care could change the current practice of pathology,” said lead researcher Rebecca Richards-Kortum, Rice’s Malcolm Gillis University Professor and professor of bioengineering and of electrical and computer engineering. “We have developed a faster means to classify benign and malignant human breast tissues using fresh samples and thereby removing the need for time-consuming tissue preparation.”

    Today, breast-cancer diagnosis is an intricate process. Tissue first must be obtained, typically by either a core needle biopsy or surgical excision. Next, pathologists must complete a complex process to prepare the tissue for analysis and histological assessment.

    When examined under a microscope, cancerous and precancerous cells typically appear different from healthy cells. The study of cellular structures is known as histology, and a histological analysis is typically required for an accurate diagnosis of both the type and stage of a cancerous tumor.

    The software developed in Richards-Kortum’s lab allows for an automated histological assessment of breast cancer from tissue samples without the need for complex tissue-sample preparation or assessment by a pathologist. The software uses high-speed optical microscopy of intact breast tissue specimens.

    “We performed our analysis without tissue fixation, cutting and staining and achieved comparable classification with current methods,” Richards-Kortum said. “This cuts out the tissue-preparation process and allows for rapid diagnosis. It is also reliant on measurable criteria, which could reduce subjectivity in the evaluation of breast histology.”

    The software uses images from a confocal fluorescence microscope to analyze freshly cut human breast tissue samples for certain histological parameters that are typically used in breast cancer diagnosis. The software uses the parameter data to classify the tissue in each image and make a determination whether the imaged tissue is benign or malignant.

    Although the software could have substantial clinical relevance, Richards-Kortum said more research and refinement of the classification procedures are needed before the software can be used in a clinical setting.

    Rice graduate student Jessica Dobbs, the study’s lead author, said, “We are excited about the possibility of using these imaging techniques to improve access to histologic diagnosis in developing regions that lack the human resources and equipment necessary to perform standard histologic assessment.”

    See the full article here.

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    In his 1912 inaugural address, Rice University president Edgar Odell Lovett set forth an ambitious vision for a great research university in Houston, Texas; one dedicated to excellence across the range of human endeavor. With this bold beginning in mind, and with Rice’s centennial approaching, it is time to ask again what we aspire to in a dynamic and shrinking world in which education and the production of knowledge will play an even greater role. What shall our vision be for Rice as we prepare for its second century, and how ought we to advance over the next decade?

    This was the fundamental question posed in the Call to Conversation, a document released to the Rice community in summer 2005. The Call to Conversation asked us to reexamine many aspects of our enterprise, from our fundamental mission and aspirations to the manner in which we define and achieve excellence. It identified the pressures of a constantly changing and increasingly competitive landscape; it asked us to assess honestly Rice’s comparative strengths and weaknesses; and it called on us to define strategic priorities for the future, an effort that will be a focus of the next phase of this process.

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