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  • richardmitnick 7:53 am on June 10, 2016 Permalink | Reply
    Tags: , , scientists discover biomarkers that could help give cancer patients better survival estimates, , Using big data   

    From UCLA: “Using big data, scientists discover biomarkers that could help give cancer patients better survival estimates” 

    UCLA bloc

    UCLA

    June 09, 2016
    Stuart Wolpert

    1
    A SURVIV analysis of breast cancer isoforms developed at UCLA. Blue lines are associated with longer survival times, and magenta lines with shorter survival times. Courtesy of Yi Xing

    People with cancer are often told by their doctors approximately how long they have to live, and how well they will respond to treatments, but what if there were a way to improve the accuracy of doctors’ predictions?

    A new method developed by UCLA scientists could eventually lead to a way to do just that, using data about patients’ genetic sequences to produce more reliable projections for survival time and how they might respond to possible treatments. The technique is an innovative way of using biomedical big data — which gleans patterns and trends from massive amounts of patient information — to achieve precision medicine — giving doctors the ability to better tailor their care for each individual patient.

    The approach is likely to enable doctors to give more accurate predictions for people with many types of cancers. In this research, the UCLA scientists studied cancers of the breast, brain (glioblastoma multiforme, a highly malignant and aggressive form; and lower grade glioma, a less aggressive version), lung, ovary and kidney.

    In addition, it may allow scientists to analyze people’s genetic sequences and determine which are lethal and which are harmless.

    The new method analyzes various gene isoforms — combinations of genetic sequences that can produce an enormous variety of RNAs and proteins from a single gene — using data from RNA molecules in cancer specimens. That process, called RNA sequencing, or RNA-seq, reveals the presence and quantity of RNA molecules in a biological sample. In the method developed at UCLA, scientists analyzed the ratios of slightly different genetic sequences within the isoforms, enabling them to detect important but subtle differences in the genetic sequences. In contrast, the conventional analysis aggregates all of the isoforms together, meaning that the technique misses important differences within the isoforms.

    2
    Yi Xing. Courtesy of Yi Xing

    SURVIV (for “survival analysis of mRNA isoform variation”) is the first statistical method for conducting survival analysis on isoforms using RNA-seq data, said senior author Yi Xing, a UCLA associate professor of microbiology, immunology and molecular genetics. The research is published today in the journal Nature Communications.

    The researchers report having identified some 200 isoforms that are associated with survival time for people with breast cancer; some predict longer survival times, others are linked to shorter times. Armed with that knowledge, scientists might eventually be able to target the isoforms associated with shorter survival times in order to suppress them and fight disease, Xing said.

    The researchers evaluated the performance of survival predictors using a metric called C-index and found that across the six different types of cancer they analyzed, their isoform-based predictions performed consistently better than the conventional gene-based predictions.

    The result was surprising because it suggests, contrary to conventional wisdom, that isoform ratios provide a more robust molecular signature of cancer patients than overall gene abundance, said Xing, director of UCLA’s bioinformatics doctoral program and a member of the UCLA Institute for Quantitative and Computational Biosciences.

    “Our finding suggests that isoform ratios provide a more robust molecular signature of cancer patients in large-scale RNA-seq datasets,” he said.

    The researchers studied tissues from 2,684 people with cancer whose samples were part of the National Institutes of Health’s Cancer Genome Atlas, and they spent more than two years developing the algorithm for SURVIV.

    According to Xing, a human gene typically produces seven to 10 isoforms.

    “In cancer, sometimes a single gene produces two isoforms, one of which promotes metastasis and one of which represses metastasis,” he said, adding that understanding the differences between the two is extremely important in combatting cancer.

    “We have just scratched the surface,” Xing said. “We will apply the method to much larger data sets, and we expect to learn a lot more.”

    Co-authors of the research are lead author Shihao Shen, a senior research scientist in Xing’s laboratory; Ying Nian Wu, a UCLA professor of statistics; Yuanyuan Wang, and Chengyang Wang, UCLA doctoral students.

    The research was funded by the National Institutes of Health (grants R01GM088342 and R01GM105431) and the National Science Foundation (grant DMS1310391). Xing’s research is also supported by an Alfred Sloan Research Fellowship.

    See the full article here .

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    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.

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  • richardmitnick 9:01 am on June 9, 2016 Permalink | Reply
    Tags: , , Scientists identify drugs to target ‘Achilles heel’ of Chronic Myeloid Leukaemia cells, U Glasgow   

    From U Glasgow: “Scientists identify drugs to target ‘Achilles heel’ of Chronic Myeloid Leukaemia cells” 

    U Glasgow bloc

    University of Glasgow

    08 Jun 2016
    ali.howard@glasgow.ac.uk
    0141 330 6557

    elizabeth.mcmeekin@glasgow.ac.uk
    0141 330 4831

    New research, by the Universities of Glasgow and Manchester, has revealed an ‘Achilles heel’ of Chronic Myeloid Leukaemia (CML) and found drugs to successfully target this weakness and eradicate the disease in mice.

    The study*, which is published in Nature today, analysed both CML and normal blood stem cells and found two proteins that were key to the survival of CML stem cells. The group, which has been working on this research for more than six years, then developed a drug combination to simultaneously target these critical proteins and kill the cancer stem cells, while largely sparing normal cells.

    The interdisciplinary research team, led by Professor Tessa Holyoake from the University of Glasgow and Professor Tony Whetton from the University of Manchester, used a range of techniques to show that these two proteins (p53 and c-Myc) act as ‘gateway controllers’ in CML.

    Guided by the concept of precision medicine (the right drug, at the right time, for the right effect in the patient), the team designed a new treatment to exploit this critical weakness in the cancer. Using CML cells transplanted into mice, the authors demonstrated that drugs targeting these two proteins killed the cells that cause the leukaemia, effectively eradicating the disease.

    The results have potential implications for other cancers including acute myeloid leukaemia and brain tumours. The researchers are now keen to build on their work by beginning human trials in patients with drug-resistant CML.

    Professor Holyoake, who led the team from the Paul O’Gorman Leukaemia Research Centre, said: “We are certainly excited by the results shown in the study. The research – a fantastic example of precision medicine in action – is at an early stage, but the data we collected has revealed two weaknesses in CML and a potential drug approach to eradicating these key stem cells.

    “We also could not have achieved such an excellent result without all the generous stem cell donations from both CML patients and other members of the public, so it is important to say thank you to them.”

    The team used a range of techniques in their research including proteomics (the large scale study of quantities, structures and functions of proteins).

    Professor Whetton said: “We have found a way to kill leukaemia stem cells which could lead to a cure of chronic myeloid leukaemia instead of managing the disease. We are really excited that our new proteomics approaches helped to achieve this.

    “There are so many other diseases where we can use the same proteomics approach to find precision medicine solutions for patients. We have the largest clinical proteomics centre in Europe in Manchester so we really look forward to contributing to this work.”

    Current therapy for CML is with tyrosine kinase inhibitors (TKIs) which effectively hold back the disease, but do not cure it. If the therapy is stopped, the leukaemia relapses in the majority of patients, requiring CML patients to remain on treatment for their lifetime. These drugs, as well as being costly to administer, can cause a number of side effects including diabetes and vascular problems. It is the dual issues of cost and toxicity in current CML treatment that has driven this particular piece of research.

    Dr Matt Kaiser, Head of Research at Bloodwise, said: “Advances made in treatment for this type of leukaemia have, thanks to research, been one of the great medical success stories of recent years, with the transformation of a usually fatal cancer into a lifelong manageable condition for most patients. The only hope of a permanent cure at the moment is a gruelling stem cell transplant, which doesn’t always work and would not be suitable for many patients to even consider. Although it’s early days, these hugely significant findings suggest that targeted drugs could be developed to cut the cancer off at its roots while sparing healthy cells, providing hope of more effective and kinder treatments.”

    Dr Áine McCarthy, senior science information officer at Cancer Research UK, said: “By recognising the important roles p53 and MYC play in helping chronic myeloid leukaemia stem cells to survive, this study has identified two new ways to target and kill these cells. Excitingly, this early-stage laboratory work also showed that two experimental drugs which target the effects of these molecules can kill CML stem cells in mice. The next step will be to test if this combination works the same way in people, and if it is safe to use.”

    The study, ‘Dual targeting of p53 and c-Myc selectively eliminates leukaemic stem cells’ is published in Nature. The research was funded by Bloodwise, Cancer Research UK, The Howat Foundation, Roche, Constellation Pharmaceuticals, the Medical Research Council (MRC), the Scottish Government Chief Scientist Office, Friends of Paul O’Gorman, and the British Society for Haematology start-up fund.

    About the Research

    The research team used an unbiased approach to their work, which involved a series of laboratory tests complemented with computational analyses and proteomics. Human stem cell samples were collected from CML donors and tested against donated stem cells from healthy individuals.

    After gathering protein and RNA data from CML and healthy cell types, they used computational analyses to identify the likely protein interactions controlling CML stem cells. The proteins p53 and c-Myc were revealed as controllers in cancer but not in the normal stem cells. Using CML cells transplanted into mice they demonstrated that drugs targeting this dual hub killed the CML stem cells.

    About CML

    CML is a blood cancer affecting less than 1% of the population with more than 700 new patients diagnosed in the UK each year. It causes the body to make too many white blood cells, which over time fill the bone marrow and reduce the number of healthy white blood cells.

    As a result of CML sufferers surviving longer (85% live for more than five years after being diagnosed) there is a growing economic cost associated with current therapy costing between 40,000 and 70,000 Euros for one patient per year in Europe.

    CML was also the first cancer found to have a genetic mutation. As a result science has used CML as a learning model to understand how other cancers work, and importantly how patients become resistant to drug therapy.

    *Science paper:
    There is no link to the science paper in the article. I have requested a link. If I get a link I will update the article.

    See the full article here .

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    U Glasgow campus

    The University of Glasgow (Scottish Gaelic: Oilthigh Ghlaschu, Latin: Universitas Glasguensis) is the fourth oldest university in the English-speaking world and one of Scotland’s four ancient universities. It was founded in 1451. Along with the University of Edinburgh, the University was part of the Scottish Enlightenment during the 18th century. It is currently a member of Universitas 21, the international network of research universities, and the Russell Group.

    In common with universities of the pre-modern era, Glasgow originally educated students primarily from wealthy backgrounds, however it became a pioneer[citation needed] in British higher education in the 19th century by also providing for the needs of students from the growing urban and commercial middle class. Glasgow University served all of these students by preparing them for professions: the law, medicine, civil service, teaching, and the church. It also trained smaller but growing numbers for careers in science and engineering.[4]

    Originally located in the city’s High Street, since 1870 the main University campus has been located at Gilmorehill in the West End of the city.[5] Additionally, a number of university buildings are located elsewhere, such as the University Marine Biological Station Millport on the Island of Cumbrae in the Firth of Clyde and the Crichton Campus in Dumfries.

    Alumni or former staff of the University include philosopher Francis Hutcheson, engineer James Watt, philosopher and economist Adam Smith, physicist Lord Kelvin, surgeon Joseph Lister, 1st Baron Lister, seven Nobel laureates, and two British Prime Ministers.

     
  • richardmitnick 8:18 am on June 9, 2016 Permalink | Reply
    Tags: , , , Scientists have performed the first trials of a 'universal cancer vaccine'   

    From Science Alert: “Scientists have performed the first trials of a ‘universal cancer vaccine’ “ 

    ScienceAlert

    Science Alert

    2 JUN 2016
    FIONA MACDONALD

    1
    Cancer Research UK via Henry Scowcroft/YouTube

    It’s really happening.

    Scientists just took a big, “very positive” step towards developing what could be the first ‘universal cancer vaccine’.

    The results from early trials in humans, along with research in mice, have just been published, and they suggest that the new technique could be used to activate patients’ immune systems against any type of tumour, no matter where it is in the body.

    Unlike the vaccines we’re familiar with, this potential vaccine would be given to patients who already have cancer, rather than those at risk of getting it. It basically works by shooting tiny ‘darts’ containing pieces of RNA extracted from the patient’s cancer cells at the body’s own immune system, convincing them to launch an all-out attack on any tumours they come across.

    By just changing the RNA inside those darts, the team can, in theory, mobilise the immune system against any kind of cancer. “[Such] vaccines are fast and inexpensive to produce, and virtually any tumour antigen can be encoded by RNA,” the team, led by researchers at Johannes Gutenberg University of Mainz in Germany, reports in Nature.

    “Thus, the nanoparticulate RNA immunotherapy approach introduced here may be regarded as a universally applicable novel vaccine class for cancer immunotherapy.”

    Immunotherapy, which involves using the patient’s own immune system to attack cancer, isn’t in itself new – researchers are already using it against different cancer types with great results.

    But until now, researchers have mostly done this by genetically engineering special, cancer-targeting immune cells in the lab, and then injecting them back into a patient – which is a time-consuming and expensive process.

    The difference with this technique is that the vaccine is made in the lab, and it introduces the cancer DNA into the immune cells within the body, which is a lot less invasive. It also means that the vaccine can be tweaked to hunt a range of cancer types.

    So why isn’t the immune system naturally taking out these cancer types?

    “One reason is that cancer cells are similar in many ways to normal cells and the immune system avoids attacking the self,” explain Dutch immunologists Jolanda de Vries and Figdor in a commentary accompanying the Nature paper.

    That means that when you develop a vaccine, you need to use an antigen – a foreign molecule that works like a ‘mugshot’ for the immune system – that’s not expressed in normal cells, too.

    “Only relatively modest immune responses occur with vaccines containing antigens that are also expressed on healthy tissue,” write de Vries and Carl Figdor. “Strong immune responses can be expected only when cancer cells express antigens that are not usually expressed in normal adult cells.”

    It’s this kind of cancer-specific antigen that the new vaccine is designed to deliver to the immune system. It works by coating the cancer RNA in a simple, fatty acid membrane, and giving it a slightly negative charge.

    This means that once the vaccine is injected into a patient, it’s drawn via electric charge towards dendritic immune cells in the spleen, lymph nodes, and bone marrow.

    These dendritic cells then ‘show’ the cancer RNA to the body’s T cells and, to anthropomorphise the situation, pretty much tell them, “Hey, this is the guy we’re after, go get him.” The goal is that the T cells will then go out and mass murder all the cancer cells in the body.

    And this is what early research by the German team has demonstrated in mice. Once injected with the vaccine, the immune system was able to fight “aggressively growing” tumours, the research found.

    Of course, many results in mice don’t translate to humans, so we can’t get too excited just yet.

    The team has also now trialled a version of the vaccine in three patients with melanoma. The point of the trial was only to test whether the vaccine was safe to use in humans, not whether it was effective, and so far, the results are promising. The side effects were limited to flu-like symptoms, which is better than most chemotherapy treatments.

    The team is now waiting 12 months for follow-up results from this safety trial, and if all goes well, will start a larger clinical trial after that to see if the vaccine really works.

    “By combining laboratory-based studies with results from an early-phase clinical trial, this research shows that a new type of treatment vaccine could be used to treat patients with melanoma by boosting the effects of their immune systems,” Aine McCarthy, the senior science information officer at Cancer Research UK, told The Telegraph.

    “Because the vaccine was only tested in three patients, larger clinical trials are needed to confirm it works and is safe, while more research will determine if it could be used to treat other types of cancer.”

    Although it’s still very early days, we have another reason to feel hopeful about the future of cancer treatment. And that’s always a good thing.

    See the full article here .

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  • richardmitnick 7:33 am on June 9, 2016 Permalink | Reply
    Tags: , , Researchers prove lung cancer mutations can be detected in saliva,   

    From UCLA: “Researchers prove lung cancer mutations can be detected in saliva” 

    UCLA bloc

    UCLA

    June 08, 2016
    Brianna Aldrich

    1
    The EFIRM machine was developed at UCLA. EZLife BioSciTech Co., Ltd

    IMPACT

    Confirming that saliva is just as accurate as biopsied tissues to detect treatable cancer mutations is a major step forward in the field of salivary diagnostics. Collecting and analyzing saliva is a non-invasive, inexpensive method in the early detection of many types of cancer. Lung cancer patients can particularly benefit from this method as lung cancer tends to be diagnosed in advanced stages and may be mistaken for other problems.

    METHOD

    Researchers from the UCLA School of Dentistry and their collaborators performed a double-blind study on 37 people who have non-small cell lung cancer at three lung cancer centers in Chengdu, China. For each person, pre- and post-biopsy samples were collected for tissue and saliva cells. The researchers began by cataloging the biopsied plasma cells (from the lungs) using digital polymerase chain reaction. Next, the team cataloged the saliva cells using a proprietary UCLA-developed technology, called electric field-induced release and measurement (EFIRM) liquid biopsy, to see whether they could detect the same mutations as they did with the plasma cells.

    They were looking for epidermal growth factor receptor (EGFR) mutations, which are early cellular signals for cancer. More specifically, they were looking for epidermal growth factor receptor L858R and exon 19del — two types of cancer mutations.

    FINDINGS

    The team found saliva detection correctly predicted the mutations in all 37 pre- and post-surgery saliva samples with 100 percent accuracy. The biopsied tissue predicted mutations with 70 percent accuracy. Furthermore, they found that the mutation signals in saliva were cleaner than in the biopsied tissue for L858R; and the tissue and saliva samples had clean separation for exon 19del.

    “This study has confirmed the performance of EFIRM liquid biopsy using as little as 40 microliters of saliva for detecting EGFR mutations,” said Dr. David Wong, lead author on the study and the associate dean for research at the UCLA School of Dentistry. “We are confident that EFIRM liquid biopsy is just as effective at detecting cancer mutations as the current dPCR method of testing tissue. The results from this study show that we are even closer to using saliva to detect cancer mutations; and that saliva can be just as accurate as tissue.”

    BACKGROUND

    According to the World Health Organization, lung cancer is the leading cause of cancer deaths worldwide. In the United States alone, there are projected to be 225,000 new cases diagnosed in 2016. There is also a growing concern about the rise of lung cancer in women and in Asian countries where the frequency of cancer mutations is three times higher.

    The clinical gold standard for detecting non-small cell lung cancer mutations is to perform a tissue biopsy. However, performing a biopsy incurs the risk of puncturing a lung, and for elderly patients the recovery time is long and difficult.

    AUTHORS

    Other authors on the study were Fang Wei and Yong Kim from the UCLA School of Dentistry; David Chia from the UCLA Department of Pathology and Laboratory Medicine; Wei Liao from EZLife BioSciTech Co., Ltd.; Ziding Feng from the University of Texas MD Anderson Cancer Center; Dr. Youlin Qiao from Peking Union Medical College and Dr. Qinghua Zhou from Sichuan University.

    Wong is the Felix and Mildred Yip Endowed Chair in Dentistry and the director for UCLA Center for Oral/Head & Neck Oncology Research at the UCLA School of Dentistry. He is also a member of the UCLA Jonsson Comprehensive Cancer Center.

    PRESENTATION

    Wong presented the team’s findings at the American Society of Clinical Oncology’s 2016 Annual Meeting on June 4. Prototypes of point-of-care and reference lab high-throughput platforms were on display at the exhibit hall at ASCO 2016.

    DISCLOSURE

    David Wong is co-founder of RNAmeTRIX Inc., a molecular diagnostic company. He holds equity in RNAmeTRIX, and serves as a company director and scientific advisor. The University of California also holds equity in RNAmeTRIX. Intellectual property that Wong invented and which was patented by the University of California has been licensed to RNAmeTRIX. Wong is a consultant to GlaxoSmithKlein, PeriRx, Wrigley and Colgate-Palmolive.

    See the full article here .

    Please help promote STEM in your local schools.

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    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 4:01 pm on June 8, 2016 Permalink | Reply
    Tags: , , , Portable probes hunt down cancer cells during surgery   

    From EPFL: “Portable probes hunt down cancer cells during surgery” 

    EPFL bloc

    École Polytechnique Fédérale de Lausanne EPFL

    08.06.16
    Laure-Anne Pessina


    Access mp4 video here .
    Light, wireless probes the size of a large pen have been developed to identify cancer cells and suspicious lymph nodes during surgery. The probes, which EPFL helped develop, are now being tested by surgeons at the University Hospital of Lausanne (CHUV) and across Europe.

    When surgeons remove a malignant tumor, they have to be sure to get all the cancer cells. Just as crucial, they have to determine whether the tumor has already sent micrometastases into the neighboring lymph nodes on the way to the rest of the body.

    EPFL, in partnership with Forimtech and the CHUV, developed two compact, light and wireless probes that help doctors with both of these tasks. The Gamma probe improves on similar devices already in use in radioguided surgery, while the Beta probe is a totally new type of device able to detect extremely small bits of cancerous tissue.

    The two probes, measuring 20 centimeters long and weighing barely 100 grams, are easy to work with and to insert into the surgical wound. The probes guide the surgeon with auditory signals similar to those of a Geiger counter, accurately locating what the human eye often cannot see.

    Hunting down malignant cells

    The Beta probe is based on a new concept of particle detection. It identifies the presence of even minute quantities of cancer cells from the main tumor. After removing the tumor, the surgeon will use the probe to see if there is any residual cancer tissue.

    The probe works by searching for positrons, which are given off by a tracer substance that, once administered to the patient, attaches itself to cancer cells. Positrons can only travel through one millimeter of tissue. When they are found, cancer cells cannot be far away.

    The Beta probe reduces the risk of complications and helps prevent the disease from spreading further. Because it pinpoints unhealthy cells, surgeons are able to preserve as much healthy tissue as possible. The device is still in the clinical test phase. A three-year effectiveness study on 60 patients is under way at the CHUV.

    Looking for sentinel lymph nodes and metastases

    The Gamma probe represents an improvement on an existing technology. It doesn’t detect cancer cells directly, but it finds the sentinel lymph node near the main tumor. This is the lymph node that cancer cells first reach before spreading to the rest of the body. It is removed and examined by doctors to determine the stage of the disease and identify the most appropriate treatment.

    “With the Gamma probe, we can remove just the sentinel lymph node. And if it turns out to be free of cancer cells, that means the tumor hasn’t spread,” said Maurice Matter, a surgeon at the CHUV.

    The probe that EPFL helped develop is lighter, more accurate and easier to use than competing devices, and it finds the sentinel lymph node more quickly.

    Miniaturizing the electronics

    In the case of both probes, the role of EPFL’s researchers was to design the device and miniaturize the electronics. “The system has to be solid enough to withstand sterilization,” said Edoardo Charbon, the director of the Advanced Quantum Architecture Lab (AQUA). “The probe has a little window at one end that picks up the gamma rays or positrons given off by the substance injected into the patient. A scintillator converts the energy of the rays into photons, which are then detected by a highly sensitive sensor.”

    The probes, which were given the CE mark in March 2015, have already been used in around 30 operations at the CHUV. Starting this year, testing will be rolled out to hospitals across Europe.

    —–
    The probes were developed as part of a CTI project (Commission for Technology and Innovation) by three partners: Forimtech (whose founders are from CERN), which contributed its expertise in particle detection, the CHUV, which contributed its clinical expertise, and EPFL, which contributed its expertise in microelectronics and VLSI design.

    See the full article here .

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    EPFL campus

    EPFL is Europe’s most cosmopolitan technical university with students, professors and staff from over 120 nations. A dynamic environment, open to Switzerland and the world, EPFL is centered on its three missions: teaching, research and technology transfer. EPFL works together with an extensive network of partners including other universities and institutes of technology, developing and emerging countries, secondary schools and colleges, industry and economy, political circles and the general public, to bring about real impact for society.

     
  • richardmitnick 6:29 am on June 7, 2016 Permalink | Reply
    Tags: , , ,   

    From HFCC at WCG: “Help Fight Childhood Cancer Project Researchers Publish a Paper” 

    New WCG Logo

    WCGLarge

    6 Jun 2016

    Summary
    The Help Fight Childhood Cancer project searched for a cure for a particular childhood brain cancer. The researchers have found that some of the promising compounds they identified also show an antidepressant capability.

    Lay Summary:

    The Help Fight Childhood Cancer project researchers have published a paper on serendipitous results they found from the drug candidate search run on World Community Grid. The project originally searched for candidate compounds that targeted specific proteins to help cure a childhood brain cancer called neuroblastoma. Some of the targeted proteins are also involved in several psychological disorders. They have found that some of the identified compounds show an antidepressant capability. Furthermore, additional research might lead to potential treatments for Huntington’s disease and Alzheimer’s disease. The paper was published in the journal Neurochemistry International.

    Paper title: Effects of novel small compounds targeting TrkB on neuronal cell survival and depression-like behavior

    Authors: Mayu Fukuda, Atsushi Takotori, Yohko Nakamura, Akiko Suganami, Tyuji Hoshino, Yutaka Tamura, Akira Nakagawara

    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.

    BOINCLarge

    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-
    OpenZika

    Rutgers Open Zika
    Zika

    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 8:02 pm on June 6, 2016 Permalink | Reply
    Tags: , Biden Unveils Major Database to Advance Cancer Research, , Genomic Data Commons (GDC),   

    From SA: “Biden Unveils Major Database to Advance Cancer Research” 

    Scientific American

    Scientific American

    June 6, 2016
    Bill Berkrot

    1
    VP Joe Biden. Credit: Marc Nozell/Flickr, CC BY 2.0

    A new unified system to facilitate sharing of genomic and clinical data among cancer researchers to help promote advances in personalized treatment for the many forms of the disease was launched on Monday, the U.S. National Cancer Institute said.

    Details of the project, known as Genomic Data Commons (GDC), were set to be announced by U.S. Vice President Joe Biden at the American Society of Clinical Oncology meeting in Chicago.

    GDC, with an operation center at the University of Chicago, will be a key component of President Obama’s “national cancer moonshot” effort to find cures and his Precision Medicine Initiative, NCI said.

    The project will receive funding from $70 million allocated to NCI for cancer genomics projects under the precision medicine initiative, which involves efforts to use advanced genetic information to match individual patients with treatments most likely to help their particular type of cancer.

    More and more medicines are being developed that address specific genetic mutations associated with a variety of cancers and tumor types.

    GDC will centralize, standardize and make accessible data from large-scale NCI programs such as The Cancer Genome Atlas and an equivalent database for childhood cancers, considered among the largest cancer genomics datasets in the world. The information will be made available at no charge to any cancer researcher.

    “The GDC will also house data from a number of newer NCI programs that will sequence the DNA of patients enrolled in NCI clinical trials,” Dr. Louis Staudt of NCI said in a statement.

    Georgetown University data scientist Subha Madhavan, who was not involved in the GDC, welcomed the project, given the complexity and vast amounts of information involved.

    “The irony of individualized treatment for one patient is that we have to manage billions of bits of information from thousands of others,” Madhavan said in a statement.

    “The selection of a precise cancer therapy based on a patient’s molecular profile requires computer-assisted analysis of enormous molecular, clinical, patient history, and pharmacological datasets that often come from very disparate and heterogeneous data sources,” she added.

    Data in the GDC, representing thousands of cancer patients and tumors, will be harmonized using standardized software algorithms so that they are accessible and broadly useful to researchers, NCI said.

    See the full article here .

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    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 2:54 pm on June 6, 2016 Permalink | Reply
    Tags: , , Cancer Institute of New Jersey,   

    From Rutgers: “Investigational Immunotherapy Drug Well Tolerated in those with Rare Form of Melanoma” 

    Rutgers University
    Rutgers University

    June 6, 2016

    Michele Fisher
    732-235-9872
    michele.fisher@rutgers.edu

    Research from Rutgers Cancer Institute of New Jersey investigator and worldwide colleagues examines patients with Merkel cell carcinoma in phase II clinical trial

    An investigational immunotherapy drug being tested in the treatment of a rare form of skin cancer known as Merkel cell carcinoma has been found to be well tolerated with a clinical benefit seen in up to 42 percent of patients who failed prior treatment and were observed for at least six months. That’s according to research from a Rutgers Cancer Institute of New Jersey physician scientist and colleagues across the globe that is being presented at the American Society of Clinical Oncology Annual Meeting being held in Chicago this week. The study is believed to be the largest trial to date investigating the programmed death-1 receptor ligand (PD-L1) in this form of cancer.

    Immunotherapies harness the body’s natural defenders, T-cells, in fighting a disease like cancer. T-cells can be looked at as a car that crashes into cancer cells. PD-L1 is a brake on the car that prevents it from crashing. The immunotherapy drug avelumab examined in this study allows that brake to be released, allowing T-cells to do their job in attacking the disease – in this case, Merkel cell carcinoma.

    Merkel cell carcinoma is a sun exposure-related form of skin cancer that is more aggressive than melanoma affecting 1,500 people each year in the United States and according to the National Cancer Institute, the number of cases diagnosed each year is on the rise. The five-year survival rate for this disease is approximately 60 percent and is only 20 percent for those with disease that has spread to other parts of the body (metastatic). “Chemotherapy and radiation are not associated with long-term, overall survival, and this form of cancer is uniformly fatal, especially for those with metastatic disease. With that, there is clearly an unmet need for treatment options in this population,” says the study’s lead investigator Howard L. Kaufman, MD, FACS, associate director for clinical science and chief surgical officer at Rutgers Cancer Institute of New Jersey. Dr. Kaufman and colleagues examined patients with metastatic disease.

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    Dr. Howard L. Kaufman

    The study enrolled 88 patients, whose metastatic Merkel cell carcinoma progressed after receiving first or second line chemotherapy. Participants received a 10 mg/kg dose of avelumab every two weeks. Participants were followed for a median of 10 months. Investigators found 32 percent of patients achieved a complete or partial response (eight complete, 20 partial) and another 10 percent (nine patients) achieved stable disease. The findings also showed tumor responses to be rapid, with 22 of 28 patients (78.6 percent) responding to avelumab within seven weeks of starting therapy. A durable response was shown with 23 of 28 patients (82.1 percent) still responding at the time of analysis. Treatment-related adverse events were low grade (Grade 1 or 2) and seen in 62 patients (70.5 percent). The most common was fatigue (23.9 percent). Grade 3 adverse events were seen in four patients (4.5 percent) and included two cases of a reduction in lymphocytes in the blood and three cases of laboratory abnormalities relating to increased liver enzymes, blood cholesterol and blood creatine kinase. There were no Grade Four adverse events or death related to treatment.

    “The typical patient with metastatic Merkel cell is a male in his mid-70s and often with co-morbid disease. A lot of patients in this population are unable to tolerate chemotherapy. Those who are may not see a response for up to three months, and side effects are likely. Our study shows the response to avelumab is not only durable for some patients but also rapid, which translates into a manageable quality of life for them,” says Kaufman. “Yes, it may be a minor inconvenience to undergo an infusion for the treatment, but we’re seeing patients leaving the clinic feeling well and heading out to normal activities like shopping or dinner – not something we often see after chemotherapy is administered. The safety profile is remarkable. Side effects are easily managed and consistent with anti-PD-L1 antibodies in other tumor types,” notes Kaufman. The team did report Grade 1 or 2 infusion reactions to avelumab in 17 percent of patients, but Kaufman notes that this was controlled, and in many cases could be prevented with pre-infusion medications.

    Carrie Best of Ohio is believed to be the first patient globally to take avelumab as part of a clinical trial for Merkel cell carcinoma. A school psychologist with a young son, Best was diagnosed in her late 40s with an advanced form of disease in 2014 and was told by her community oncologist that her odds of recovery were “less than one percent.” She researched her disease and met the criteria for the avelumab study led locally by Kaufman at Rutgers Cancer Institute of New Jersey. “After enduring various treatments including chemotherapy and a clinical trial leaving me physically and mentally exhausted, I wasn’t sure what to expect with an investigational therapy,” notes Best. “While on avelumab, I was able to get around easier, ride my bike and go to the park with my little boy. I started feeling relatively ‘normal.’ Six weeks after my first treatment, Dr. Kaufman told me my scans were clear and there was no evidence of disease. It was probably the most defining and powerful moment in my life, especially as I realized the improved quality of life I was afforded while receiving treatment. It was amazing to me that while I was in my most desperate hour, I was able to continue with the things most important to me – being a wife and an active participant in my child’s life, working in a job I love and being productive. I am truly grateful that other patients with advanced stage disease may have an opportunity to experience similar outcomes.”

    “A decade ago we might have one patient in my clinic with this type of advanced disease responding to treatment. Today, we have an opportunity for many more patients to respond with ‘T-cell checkpoint inhibitor’ drugs,” notes Kaufman. “This study shows meaningful results and adds to emerging data showing promise with immunotherapy drugs in other forms of cancer.”

    The trial was sponsored by Merck KGaA, Darmstadt, Germany and is part of an alliance between Merck KGaA and Pfizer, Inc.

    About Rutgers Cancer Institute of New Jersey

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    Rutgers Cancer Institute of New Jersey (http://www.cinj.org) is the state’s only National Cancer Institute-designated Comprehensive Cancer Center. As part of Rutgers, The State University of New Jersey, the Cancer Institute of New Jersey is dedicated to improving the detection, treatment and care of patients with cancer, and to serving as an education resource for cancer prevention. Physician-scientists at Rutgers Cancer Institute engage in translational research, transforming their laboratory discoveries into clinical practice. To make a tax-deductible gift to support the Cancer Institute of New Jersey, call 848-932-8013 or visit http://www.cinj.org/giving. Follow us on Facebook at http://www.facebook.com/TheCINJ.

    The Cancer Institute of New Jersey Network is comprised of hospitals throughout the state and provides the highest quality cancer care and rapid dissemination of important discoveries into the community. Flagship Hospital: Robert Wood Johnson University Hospital. System Partner: Meridian Health (Jersey Shore University Medical Center, Ocean Medical Center, Riverview Medical Center, Southern Ocean Medical Center, and Bayshore Community Hospital). Affiliate Hospitals: JFK Medical Center, Robert Wood Johnson University Hospital Hamilton (CINJ Hamilton), and Robert Wood Johnson University Hospital Somerset.

    See the full article here .

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    Rutgers, The State University of New Jersey, is a leading national research university and the state’s preeminent, comprehensive public institution of higher education. Rutgers is dedicated to teaching that meets the highest standards of excellence; to conducting research that breaks new ground; and to providing services, solutions, and clinical care that help individuals and the local, national, and global communities where they live.

    Founded in 1766, Rutgers teaches across the full educational spectrum: preschool to precollege; undergraduate to graduate; postdoctoral fellowships to residencies; and continuing education for professional and personal advancement.

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  • richardmitnick 2:25 pm on June 3, 2016 Permalink | Reply
    Tags: , , Celebrex fights cancer,   

    From Scripps: “Scientists Show Commonly Prescribed Painkiller Slows Cancer Growth” 

    Scripps
    Scripps Research Institute

    June 06, 2016
    By Eric Sauter

    Scientists from the Florida campus of The Scripps Research Institute (TSRI) have found that one of the most widely prescribed pain and anti-inflammation drugs slows the growth rate of a specific kind of cancer in animal models and suggests the medication could have the same effect on other types of tumors.

    The new study, published online ahead of print by the journal Cancer Research, focused on the effects of celecoxib (Pfizer’s Celebrex®).

    Celebrex® targets an enzyme called “cyclooxygenase-2” (COX-2), which is linked to pain and inflammation. This enzyme is also critical in the creation of prostaglandins, compounds that act like hormones and play a role in promoting tumor growth. COX-2 expression is typically low in normal tissue, but high in multiple types of cancers.

    “We were actually interested in determining what a particular signaling pathway does in cancer,” said TSRI Associate Professor Joseph Kissil, who led the study. “In the process, we found that it activates genes that promote survival of tumor cells and that they do so by turning on enzymes involved in inflammation, including COX2, which anti-inflammatory drugs like Celebrex® inhibit.”

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    Authors of the new study included (left to right) Smitha Kota, William Guerrant, Joseph Kissil, Scott Troutman and Vinay Mandati.

    The researchers went on to conduct animal studies tracking the effects of celecoxib on the growth of cancer cells from a tumor type known as neurofibromatosis type II (NF2). In humans, NF2 is a relatively rare inherited form of cancer caused by mutations in the anti-tumor gene NF2, which leads to benign tumors of the auditory nerve.

    Animals received a daily dose of the drug, and tumor growth was followed by imaging. Analysis of the results showed a significantly slower tumor growth rate in celecoxib-treated models than in controls.

    Using various approaches, the new study also showed that a signaling cascade known as the Hippo-YAP pathway is involved in these results and that the protein YAP is required for the proliferation and survival of NF2 cells and tumor formation.

    “Our study shows that COX2 inhibitors do have an effect on the tumor cells,” said TSRI Research Associate William Guerrant, the study’s first author. “They also have an impact on inflammatory responses that play a role in tumor growth. It’s possible that in other cancers these effects might actually be stronger because of the drug’s impact on inflammation.”

    In addition to Kissil and Guerrant, other authors of the study, “YAP Mediates Tumorigenesis in Neurofibromatosis Type 2 by Promoting Cell Survival and Proliferation through a COX-2–EGFR Signaling Axis,” are Smitha Kota, Scott Troutman, Vinay Mandati and Mohammad Fallahi of TSRI; and Anat Stemmer-Rachamimov of Massachusetts General Hospital.

    The work was supported by the National Institutes of Health (grants NS077952 and CA124495). Guerrant is also a recipient of a Young Investigator Award from the Children’s Tumor Foundation.

    See the full article here .

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    The Scripps Research Institute (TSRI), one of the world’s largest, private, non-profit research organizations, stands at the forefront of basic biomedical science, a vital segment of medical research that seeks to comprehend the most fundamental processes of life. Over the last decades, the institute has established a lengthy track record of major contributions to the betterment of health and the human condition.

    The institute — which is located on campuses in La Jolla, California, and Jupiter, Florida — has become internationally recognized for its research into immunology, molecular and cellular biology, chemistry, neurosciences, autoimmune diseases, cardiovascular diseases, virology, and synthetic vaccine development. Particularly significant is the institute’s study of the basic structure and design of biological molecules; in this arena TSRI is among a handful of the world’s leading centers.

    The institute’s educational programs are also first rate. TSRI’s Graduate Program is consistently ranked among the best in the nation in its fields of biology and chemistry.

     
  • richardmitnick 1:01 pm on June 3, 2016 Permalink | Reply
    Tags: , , Cornering Cancer,   

    From MIT Spectrum: “Cornering Cancer” 


    MIT News

    1

    Spring 2016
    Leda Zimmerman

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    An illustration for the team’s March publication in Cell depicts possible paths of tumor evolution in relation to hills (presenting resistance to a drug), and valleys (sensitivity). Artwork: Boyang Zhao

    Cancers are shape shifters. A single tumor often features multiple varieties of wildly proliferating cells, with each variety undergoing genetic mutations. Chasing these moving targets, researchers tailor therapies that arrest—but only rarely vanquish—the disease.

    However, momentum may finally be shifting in the quest for effective cancer treatments.

    “For so long, therapy has been reactive,” says Michael Hemann, who has joined forces with fellow MIT faculty member Douglas Lauffenburger to address this challenge. “What if we could instead steer tumors toward an outcome we know how to manage, or toward becoming better behaving tumors?”

    This is no wishful thinking. Hemann is professor of biology at MIT’s David H. Koch Institute for Integrative Cancer Research, which has just celebrated its fifth anniversary. He and Koch Institute extramural faculty member Lauffenburger—the Ford Professor of Biological Engineering, Chemical Engineering, and Biology, and head of MIT’s Department of Biological Engineering—have been collaborating on studies that suggest it is possible to predict and shape a cancer’s unique trajectory, and to determine points along that journey when it may be especially susceptible to treatment.

    Their work, in a field of research called systems biology, creates a finely detailed portrait of the complex evolution and drug responsiveness of certain kinds of cancer.

    “Only by embracing and comprehending the complexity can you hope to come up with effective treatment,” says Lauffenburger. “And we have the experimental tools to be as comprehensive about studying complexity as we want.”

    Hemann arrived at MIT in 2006 skilled in the latest methods for manipulating genes in living organisms. As a graduate student at Johns Hopkins University, and then as a postdoctoral fellow at Cold Spring Harbor Laboratory, he had trained to use viruses and RNA interference to grow specific cancers in mice. He more recently added CRISPR to his repertoire, an even faster technique for modifying the genome of living cells.

    “We have an entirely new toolset for manipulating genetic systems in vivo,” says Hemann. “We can now perform big genetic screens with mouse models, looking at lots of phenotypes [expression of genetic traits], introducing many changes at once to see how a tumor emerges or resists a cancer therapy.”

    These kinds of experiments generate reams of genetic data that require sophisticated analysis—an area that falls directly in Lauffenburger’s wheelhouse. On the MIT faculty since 1995, Lauffenburger calls himself “half cell biologist, half engineer,” and was prepared when “biology hit the omics era.” (“Omics” refers collectively to the study of genes and proteins that comprise living organisms.)

    With research interests in cancer and biomedical engineering, Lauffenburger devises computational strategies for capturing changes within complex biological systems from the molecular level up. By “creating conceptual frameworks,” Lauffenburger says, he aims “to get the most power out of omics experimental methods.”

    “The unexpected can be transformational”

    With their common interests and complementary skillsets, Hemann and Lauffenburger seem like an obvious research match. But they needed a well-placed nudge to forge a union. This was delivered in 2008 by Justin Pritchard PhD ’12, then a graduate student of Lauffenburger’s, who was intrigued by the cancer data flowing out of Hemann’s lab. “This situation is the epitome of MIT,” says Lauffenburger. “It’s the brilliant, fearless, creative graduate students who find connections between labs.” They “facilitate our interaction in a deep way,” adds Hemann. “Students are the glue that holds us together.”

    In the course of investigating how combinations of drugs worked on B-cell lymphoma, a type of blood cancer, Hemann had generated a very large data set. “In Mike’s world, you can perturb hundreds to thousands of gene products,” says Lauffenburger. “The issue is figuring out what’s important to tumor biology.”

    Based on decades of experience treating patients, clinicians have discerned that some drugs in combination can achieve a kind of one-two punch against B-cell lymphoma. But the biological mechanisms behind their efficacy remained unknown. Pritchard realized that by using Lauffenburger’s computational models, he could mine the giant data set for patterns of drug impacts, gleaning likely pathways of tumor susceptibility, and identifying which drugs worked best, and in what combination.

    Pritchard’s research “gave a multivariate genetic foundation” to a common clinical practice, says Lauffenburger, helping provide “a biological rationale for this kind of drug treatment.”

    This study, the basis for Pritchard’s thesis and multiple journal articles, was the launching point for a series of collaborative ventures between Lauffenburger and Hemann—all facilitated by graduate students. It is a partnership that is taking both labs into new scientific territory, and breaking new ground in cancer research. As Hemann puts it: “In biology, the unexpected can be transformational.”

    The two laboratories began to zero in on what Hemann calls “one of the essential problems in cancer biology”: tumor heterogeneity. While tumor cells start as single cells, they begin growing uncontrollably, and then differentiate into diverse subpopulations. There can be heterogeneity of tumors across patients with the same cancer, as well as heterogeneity within the same tumor.

    Given such wild variation in a given type of cancer, how do researchers identify effective treatments, especially when the treatments themselves promote mutations and further drug resistance?

    “Now we can stay ahead of the game”

    Another joint graduate student, Boyang Zhao PhD ’16, began to crack this puzzle. In Hemann’s lab, he created heterogeneous lymphoma tumors in mice, and then tested these tumors with single and combination drug therapies. Zhao used Lauffenburger’s computational tools to analyze data comprised of 10,000 heterogeneous tumor compositions and their response to six drugs.

    “The computational work allowed Bo to simulate an evolving mix of tumor cells, so he could predict the response of these heterogeneous cells to treatment,” says Hemann. “This really moved us forward.”

    The team’s focus on heterogeneity began paying off rapidly. Using mouse models of acute lymphoblastic leukemia, Zhao discovered that at an early stage of the evolution of the cancer, it developed an acute sensitivity to drugs that had demonstrated no previous efficacy in the treatment of this disease. “This is the awkward phase, the teen years, for the tumor, when it’s hypersensitive to drugs,” says Hemann.

    This research suggests not only that modeling can predict optimal times for treating this leukemia, but that it might also be possible to dynamically modify cancers in order to sensitize them to therapy. “Now we can stay ahead of the game,” says Lauffenburger. “We know at what point to hit the cancer with a new drug.”

    These findings, published in the March 24, 2016, issue of the journal Cell, have the potential to improve treatment for a range of blood cancers, including acute myeloid leukemia, with its diversity of genetic subpopulations, and others such as chronic myelogenous leukemia, where only patients with a specific genetic mutation find relief through a highly targeted drug regimen.

    But the team’s hybrid approach, combining genetic manipulation in vivo and powerful computational frameworks, has even broader potential. “We believe it could apply to any type of heterogeneous cancer, which really means any type of cancer,” says Lauffenburger. “It leads us to a new world of drug screening,” adds Hemann. “We can now determine a tumor’s unexpected sensitivities, and find new compounds that have efficacy during the evolution of the disease.”

    While their work raises the possibility of rapid testing of new and more targeted cancer drugs, it also points to better application of current drugs. “If we could block the protective signals in some tumors that make them drug resistant, and find the best time to administer the drug, then current frontline chemotherapy could work better at lower doses,” says Hemann. “Our big mission is to make therapies more effective and less toxic.”

    To that end, the researchers will be partnering with clinicians at local teaching hospitals. “One of our next proving grounds will be drug resistance in lung cancer,” says Lauffenburger. This means expanding their collaboration: “We will be adding more students to our labs,” notes Hemann.

    It’s a prospect both scientists relish. “Our interactions are multifaceted, with the science and personal dimensions all intertwined,” says Lauffenburger.

    “We know how to defer to each other’s expertise, and this has allowed us to move in directions we never would have before,” says Hemann. “As with any good relationship, you find a situation that endures because it’s both productive and exciting.”

    See the full article here .

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    The mission of MIT is to advance knowledge and educate students in science, technology, and other areas of scholarship that will best serve the nation and the world in the twenty-first century. We seek to develop in each member of the MIT community the ability and passion to work wisely, creatively, and effectively for the betterment of humankind.

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