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  • richardmitnick 3:27 pm on June 25, 2017 Permalink | Reply
    Tags: Cancer, , , , , TACC Lonestar supercomputer, TACC Stampede supercomputer   

    From Science Node: “Computer simulations and big data advance cancer immunotherapy” 

    Science Node bloc
    Science Node

    09 Jun, 2017 [Where has this been?]
    Aaron Dubrow

    Courtesy National Institute of Allergy and Infectious Diseases.

    Supercomputers help classify immune response, design clinical trials, and analyze immune repertoire data.
    Scanning electron micrograph of a human T lymphocyte (also called a T cell) from the immune system of a healthy donor. Immunotherapy fights cancer by supercharging the immune system’s natural defenses (include T-cells) or contributing additional immune elements that can help the body kill cancer cells. [Credit: NIAID]

    The body has a natural way of fighting cancer – it’s called the immune system, and it is tuned to defend our cells against outside infections and internal disorder. But occasionally, it needs a helping hand.

    In recent decades, immunotherapy has become an important tool in treating a wide range of cancers, including breast cancer, melanoma and leukemia.

    But alongside its successes, scientists have discovered that immunotherapy sometimes has powerful — even fatal — side-effects.

    Identifying patient-specific immune treatments

    Not every immune therapy works the same on every patient. Differences in an individual’s immune system may mean one treatment is more appropriate than another. Furthermore, tweaking one’s system might heighten the efficacy of certain treatments.

    Scanning electron micrograph of a human T lymphocyte (also called a T cell) from the immune system of a healthy donor. Immunotherapy fights cancer by supercharging the immune system’s natural defenses (include T-cells) or contributing additional immune elements that can help the body kill cancer cells. [Credit: NIAID]

    Researchers from Wake Forest School of Medicine and Zhejiang University in China developed a novel mathematical model to explore the interactions between prostate tumors and common immunotherapy approaches, individually and in combination.

    In a study published in Nature Scientific Reports, they used their model to predict how prostate cancer would react to four common immunotherapies.

    The researchers incorporated data from animal studies into their complex mathematical models and simulated tumor responses to the treatments using the Stampede supercomputer at the Texas Advanced Computing Center (TACC).

    Dell Poweredge U Texas Austin Stampede Supercomputer. Texas Advanced Computer Center 9.6 PF

    “We do a lot of modeling which relies on millions of simulations,” says Jing Su, a researcher at the Center for Bioinformatics and Systems Biology at Wake Forest School of Medicine and assistant professor in the Department of Diagnostic Radiology.

    “To get a reliable result, we have to repeat each computation at least 100 times. We want to explore the combinations and effects and different conditions and their results.”

    TACC’s high performance computing resources allowed the researchers to highlight a potential therapeutic strategy that may manage prostate tumor growth more effectively.

    Designing more efficient clinical trials

    Biological agents used in immunotherapy — including those that target a specific tumor pathway, aim for DNA repair, or stimulate the immune system to attack a tumor — function differently from radiation and chemotherapy.

    Because traditional dose-finding designs are not suitable for trials of biological agents, novel designs that consider both the toxicity and efficacy of these agents are imperative.

    Chunyan Cai, assistant professor of biostatistics at UT Health Science Center (UTHSC)’s McGovern Medical School, uses TACC systems to design new kinds of dose-finding trials for combinations of immunotherapies.


    Writing in the Journal of the Royal Statistics Society Series C (Applied Statistics), Cai and her collaborators, Ying Yuan, and Yuan Ji, described efforts to identify biologically optimal dose combinations for agents that target the PI3K/AKT/mTOR signaling pathway, which has been associated with several genetic aberrations related to the promotion of cancer.

    After 2,000 simulations on the Lonestar supercomputer for each of six proposed dose-finding designs, they discovered the optimal combination gives higher priority to trying new doses in the early stage of the trial.

    TACC Lonestar Cray XC40 supercomputer

    The best case also assigns patients to the most effective dose that is safe toward the end of the trial.

    “Extensive simulation studies show that the design proposed has desirable operating characteristics in identifying the biologically optimal dose combination under various patterns of dose–toxicity and dose–efficacy relationships,” Cai concludes.

    Whether in support of population-level immune response studies, clinical dosing trials, or community-wide efforts, TACC’s advanced computing resources are helping scientists put the immune system to work to better fight cancer.

    See the full article here .

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    Science Node is an international weekly online publication that covers distributed computing and the research it enables.

    “We report on all aspects of distributed computing technology, such as grids and clouds. We also regularly feature articles on distributed computing-enabled research in a large variety of disciplines, including physics, biology, sociology, earth sciences, archaeology, medicine, disaster management, crime, and art. (Note that we do not cover stories that are purely about commercial technology.)

    In its current incarnation, Science Node is also an online destination where you can host a profile and blog, and find and disseminate announcements and information about events, deadlines, and jobs. In the near future it will also be a place where you can network with colleagues.

    You can read Science Node via our homepage, RSS, or email. For the complete iSGTW experience, sign up for an account or log in with OpenID and manage your email subscription from your account preferences. If you do not wish to access the website’s features, you can just subscribe to the weekly email.”

  • richardmitnick 10:27 am on June 22, 2017 Permalink | Reply
    Tags: Aneuploidy, , Cancer, , Immune system response points way to beating cancer,   

    From COSMOS: “Immune system response points way to beating cancer” 

    Cosmos Magazine bloc


    22 June 2017
    Ariella Heffernan-Marks

    A scanning electron micrograph of a cancer cell in the process of dividing.
    Steve Gschmeissner / Getty

    After so many decades of searching for a cure for cancer, new research suggests a solution might have been within our own natural immune system the whole time.

    Angelika Amon, a biologist with the Massachusetts Institute of Technology in Boston, and colleague suggest exactly this in a study published in Developmental Cell. They report finding that cells with a high level of ‘chromosome mis-segregation’ – also known as ‘aneuploidy’ – elicit an innate immune response that results in their own cell-specific death.

    If this response could be replicated in cancer cells, the researchers say, it might provide a mechanism for their successful elimination.

    Aneuploidy occurs when chromosomes do not separate evenly during cellular division. This results in a chromosomal – and therefore genetic – imbalance in the cell. DNA damage, cellular stress, metabolic defect and alterations in gene dosage can also occur.

    Many diseases and disorders have consequently been associated with aneuploidy – including 70–90% of cancer tumours. It has been suggested that alterations in gene dosage can lead to changes in cancer-driver genes, resulting in the erratic proliferation patterns seen in cancer cells.

    Despite aneuploidy being confirmed as a hallmark of cancer, however, there is still debate over the exact link. Not all tumours show the same aneuploidy phenotype, and non-cancer sufferers with aneuploidy phenotypes, such as Down syndrome, tend to demonstrate lower chances of developing cancer, according to the Koch Institute for Integrative Cancer Research, with which Amon is also associated.

    Most normal tissues do not demonstrate aneuploidy. Even mutations in chromosome-alignment proteins do not result in high numbers of aneuploid cells, according to research published in Molecules and Cells.

    Thus the question is: what happens to the aneuploid cells?

    A popular explanation has been a “p53-activated mechanism”, whereby the complex karyotype (or chromosomal arrangement) of an aneuploid cell activates the protein p53, which stimulates mitotic arrest and cell death.

    Amon and her team, however, discovered this was not the case; rather, arrest and death was the result of an innate immune system response. Using live cell imaging and immunofluorescence, they observed chromosome mis-segregation through mutating chromosome alignment proteins and recorded the time to mitotic arrest. The p53 protein was activated regardless of chromosomes being mis-segregated.

    Amon and her colleague investigated the level of DNA damage due to aneuploidy by analysing protein gamma-H2AX, which is found only during double-strand DNA breaks. Elevated levels were found in aneuploid cells, indicating significant DNA stress and damage due to chromosome mis-segregation. Immunofluorescence confirmed this was generating complex karyotypes. “These cells are in a downward spiral where they start out with a little bit of genomic mess,” Amon explains, “and it just gets worse.”

    Additional gene analysis also indicated these cells had higher levels of innate immune cells compared to normal cells. Re-exposing both normal and aneuploid cells to these factors confirmed that specific factors were acting to selectively destroy aneuploid cells – most commonly the natural killer cell NK92. It is believed this could be in response to signals from DNA damage, cellular stress or irregularities in protein levels.

    So what does this mean with regards to finding the “cure to cancer”?

    Cancer cells have found a way to evade this cellular culling strategy. If researchers can find a way to re-activate this mechanism in aneuploid cancer cells, cancer treatment could use a NK92-mediated elimination method instead of toxic and expensive radioactive therapy.

    “We have really no understanding of how that works,” Amon concedes. “If we can figure this out, that probably has tremendous therapeutic implications, given the fact that virtually all cancers are aneuploid.”

    See the full article here .

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  • richardmitnick 4:45 pm on June 20, 2017 Permalink | Reply
    Tags: , Cancer, , Petscans,   

    From TRIUMF: “Novel radiochemistry technique opens door to new PET imaging agents” 



    No image caption or credit

    A team of researchers led by SFU scientists Matthew Nodwell, Robert Britton and TRIUMF scientists Hua Yang and Paul Schaffer has demonstrated a new method for producing radioisotopes for Positron Emission Tomography (PET) cancer scans, a type of medical imaging that produces images of organs and tissues inside the body. Published on March 1st, 2017 in the Journal of the American Chemical Society (JACS), the results of the paper present an alternate methodology for incorporating the radiotracing isotope Fluorine-18 (­18F) into amino acid compounds used in PET cancer scans. This alternate route represents an exciting step towards streamlining the production of radiotracers and opens the door to diverse PET capabilities.

    PET scan is only as good as its radiotracer

    PET scans are invaluable diagnostic tools for tracking the progression of cancer and other diseases in the body. PET scans combine one of a variety of radioisotope-tagged biomolecules (‘radiotracers’), each formulated to visualize a different illness, and a gamma-ray camera to detect and locate emissions from the decaying radiotracer atoms. By tracking where the biomolecules travel and accrete within the body, PET scans can offer valuable insight into the location and degree of disease progression in real time.

    PET radioisotopes are created by ‘tagging’ a particular biomolecule with radioactive isotopes- for instance, inserting an 18F atom in the place of a hydrogen atom in an amino acid molecule. 18F is the mostly commonly used PET isotope that can be tagged to biomolecules, which in turn are chosen for their relationship to ailments like cancers, Parkinson’s, Alzheimer’s, and even broken bones.

    However, adjoining 18F to a biomolecule is no simple task. Researchers must first identify a viable molecule for insertion (one involved in the abnormal cellular metabolism characteristic of cancer, for example), then determine a location where an 18F atom can be placed without disrupting the biomolecule’s normal function. Radiochemists must then devise a precursor for that molecule and a targeted chemical reaction to insert the 18F atom. Creating new radio-tagged biomolecules is a lengthy and time-consuming exercise in synthetic chemistry, and much radiochemical research is devoted to streamlining and improving radiotracer development.

    No image caption or credit.

    The rigors of radiotracer production are, in part, why Matthew Nodwell and Hua Yang were so excited to share their results. The research group they lead, a collaboration between TRIUMF, Simon Fraser University (SFU) and the BC Cancer Agency (BCCA), has presented a new and improved way to create radiotracers via direct fluorination without the need for harsh chemical conditions or complex precursors.

    The new technique relies on the role of the amino acid leucine in cancer progression. As the building blocks of protein, amino acids often exist in high concentrations in tumours and malignancies and thus represents promising PET imaging molecules. However, traditional synthetic strategies for incorporating radionuclides into amino acid molecules often require chemically harsh conditions (strong bases, high temperatures, etc.) that risk decomposing the starting materials. Even getting the amino acid molecule to the point where it can be fluorinated can take multiple time-consuming steps involving a variety of precursor molecules. The technique developed by the group circumvents these obstacles and allows easy access to a suite of molecules that show potential for development as oncological imaging agents.

    “I think we set a new record!” said Nodwell of the new fluorination technique. “We’ve never been able to move so quickly from the first step, molecule identification, to the final step, visualizing the completed radiofluorinated tracer using a PET scan. We took a fairly unorthodox approach to the fluorination technique, but it paid off- the entire process now takes just over two weeks.”

    “Our radiofluorination technique represents a portal to access fluorinated amino acids like never before,” said Yang. “The method we’ve devised will allow rapid proof-of-feasibility for a wide variety of potential PET scanning molecules, as well as support high throughput production of radiotracers. We are eager to explore the diversity of opportunities for new oncology tracers enabled by this technique.”

    Nodwell, Yang, and members of the research group are examining the utility of their fluorination technique for developing other, non-amino acid radiotracers for other PET applications.

    See the full article here .

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    Triumf Campus
    World Class Science at Triumf Lab, British Columbia, Canada
    Canada’s national laboratory for particle and nuclear physics
    Member Universities:
    University of Alberta, University of British Columbia, Carleton University, University of Guelph, University of Manitoba, Université de Montréal, Simon Fraser University,
    Queen’s University, University of Toronto, University of Victoria, York University. Not too shabby, eh?

    Associate Members:
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  • richardmitnick 12:13 pm on June 17, 2017 Permalink | Reply
    Tags: , Cancer, , ,   

    From HMS: “Staving Off Stem Cell Cancer Risk” 

    Harvard University

    Harvard University

    Harvard Medical School

    Harvard Medical School

    April 26, 2017 [Never saw this one.]

    Image: BlackJack3D/Getty Images

    Regenerative medicine using human pluripotent stem cells to grow transplantable tissue outside the body carries the promise to treat a range of intractable disorders, such as diabetes and Parkinson’s disease.

    As stem cell lines grow in a lab dish, however, they often acquire mutations in the TP53 (p53) gene, an important tumor suppressor responsible for controlling cell growth and division, according to new research from a team at Harvard Medical School, the Harvard Stem Cell Institute and the Stanley Center for Psychiatric Research at the Broad Institute of MIT and Harvard.

    The findings suggest that genetic sequencing technologies should be used to screen stem cell cultures so that those with mutated cells can be excluded from scientific experiments and clinical therapies. If such methods are not employed, the researchers said, it could lead to an elevated cancer risk in patients receiving transplants.

    The paper, published online in the journal Nature on April 26, comes at just the right time, the researchers said, as experimental treatments using human pluripotent stem cells are ramping up across the country.

    “Our results underscore the need for the field of regenerative medicine to proceed with care,” said the study’s co-corresponding author, Kevin Eggan, a principal faculty member at HSCI and director of stem cell biology at the Stanley Center.

    The team said that the new research should not discourage the pursuit of experimental treatments, but instead should be heeded as a call to rigorously screen all cell lines for mutations at various stages of development as well as immediately before transplantation.

    “Fortunately,” said Eggan, this additional series of genetic quality-control checks “can be readily performed with precise, sensitive and increasingly inexpensive sequencing methods.”

    Hidden mutations

    Researchers can use human stem cells to recreate human tissue in the lab. Eggan’s lab in Harvard University’s Department of Stem Cell and Regenerative Biology uses human stem cells to study the mechanisms of brain disorders, including amyotrophic lateral sclerosis, intellectual disability and schizophrenia.

    Eggan has also been working with Steve McCarroll, associate professor of genetics at HMS and director of genetics at the Stanley Center, to study how genes shape the biology of neurons, which can be derived from human stem cells.

    McCarroll’s lab recently discovered a common precancerous condition in which a blood stem cell in the body acquires a so-called pro-growth mutation and then outcompetes a person’s normal stem cells, becoming the dominant generator of that person’s blood cells. People with this condition are 12 times more likely to develop blood cancer later in life.

    The current study’s lead authors, Florian Merkle and Sulagna Ghosh, collaborated with Eggan and McCarroll to test whether laboratory-grown stem cells might be vulnerable to an analogous process.

    “Cells in the lab, like cells in the body, acquire mutations all the time,” said McCarroll, co-corresponding author of the study. “Mutations in most genes have little impact on the larger tissue or cell line. But cells with a pro-growth mutation can outcompete other cells, become very numerous and ‘take over’ a tissue.”

    “We found that this process of clonal selection—the basis of cancer formation in the body—is also routinely happening in laboratories.”

    A p53 problem

    To find acquired mutations, the researchers performed genetic analyses on 140 stem cell lines. Twenty-six lines had been developed for therapeutic purposes using Good Manufacturing Practices, a quality control standard set by regulatory agencies in multiple countries. The remaining 114 were listed on the NIH registry of human pluripotent stem cells.

    “While we expected to find some mutations, we were surprised to find that about 5 percent of the stem cell lines we analyzed had acquired mutations in a tumor-suppressing gene called p53,” said Merkle.

    Nicknamed the “guardian of the genome,” p53 controls cell growth and cell death. People who inherit p53 mutations develop a rare disorder called Li-Fraumeni syndrome, which confers a near 100 percent risk of developing cancer in a wide range of tissue types.

    The specific mutations that the researchers observed are dominant negative mutations, meaning that when present on even one copy of p53, they compromise the function of the normal protein. The same dominant negative mutations are among the most commonly observed mutations in human cancers.

    “They are among the worst p53 mutations to have,” said co-lead author Ghosh.

    The researchers performed a sophisticated set of DNA analyses to rule out the possibility that these mutations had been inherited rather than acquired as the cells grew in the lab.

    Ensuring safety

    In subsequent experiments, the scientists found that p53 mutant cells outperformed and outcompeted nonmutant cells in the lab dish. In other words, a culture with a million healthy cells and one p53 mutant cell, said Eggan, could quickly become a culture of only mutant cells.

    “The spectrum of tissues at risk for transformation when harboring a p53 mutation includes many of those that we would like to target for repair with regenerative medicine using human pluripotent stem cells,” said Eggan.

    Those organs include the pancreas, brain, blood, bone, skin, liver and lungs.

    However, Eggan and McCarroll emphasized that now that this phenomenon has been found, inexpensive gene-sequencing tests will allow researchers to identify and remove from the production line cell cultures with concerning mutations that might prove dangerous after transplantation.

    The researchers point out in their paper that screening approaches already exist to identify these p53 mutations and others that confer cancer risk. Such techniques are being used in cancer diagnostics.

    In fact, an ongoing clinical trial that is transplanting cells derived from induced pluripotent stem cells (iPSCs) is using gene sequencing to ensure the transplanted cell products are free of dangerous mutations.

    This work was supported by the Harvard Stem Cell Institute, the Stanley Center for Psychiatric Research, the Rosetrees Trust, the Azrieli Foundation, the Howard Hughes Medical Institute, the Wellcome Trust, the Medical Research Council, the Academy of Medical Sciences and grants from the National Institutes of Health (HL109525, 5P01GM099117, 5K99NS08371, HG006855, MH105641).

    See the full article here .

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    HMS campus

    Established in 1782, Harvard Medical School began with a handful of students and a faculty of three. The first classes were held in Harvard Hall in Cambridge, long before the school’s iconic quadrangle was built in Boston. With each passing decade, the school’s faculty and trainees amassed knowledge and influence, shaping medicine in the United States and beyond. Some community members—and their accomplishments—have assumed the status of legend. We invite you to access the following resources to explore Harvard Medical School’s rich history.

    Harvard University campus

    Harvard is the oldest institution of higher education in the United States, established in 1636 by vote of the Great and General Court of the Massachusetts Bay Colony. It was named after the College’s first benefactor, the young minister John Harvard of Charlestown, who upon his death in 1638 left his library and half his estate to the institution. A statue of John Harvard stands today in front of University Hall in Harvard Yard, and is perhaps the University’s best known landmark.

    Harvard University has 12 degree-granting Schools in addition to the Radcliffe Institute for Advanced Study. The University has grown from nine students with a single master to an enrollment of more than 20,000 degree candidates including undergraduate, graduate, and professional students. There are more than 360,000 living alumni in the U.S. and over 190 other countries.

  • richardmitnick 11:36 am on June 15, 2017 Permalink | Reply
    Tags: , Cancer, , Low-energy ultrasound waves to trigger the dispersal of chemotherapy-containing sustained-release nanoparticles precisely at tumor sites, , ,   

    From Wyss: “A mechanical trigger for toxic tumor therapy” 

    Harvard bloc tiny
    Wyss Institute bloc
    Wyss Institute

    June 15, 2017
    Lindsay Brownell

    An electron microscope image of a hollow, roughly spherical nanoparticle aggregate (NPA), consisting of nanoparticles loaded with chemotherapy drugs. Credit: Wyss Institute at Harvard University

    Cells in nearly any part of the body can become cancerous and transform into tumors. Some, like skin cancer, are relatively accessible to treatment via surgery or radiation, which minimizes damage to healthy cells; others, like pancreatic cancer, are deep in the body and can only be reached by flooding the bloodstream with cell-killing chemotherapies that, ideally, shrink tumors by accumulating in their ill-formed blood and lymph vessels in higher amounts than in vessels of healthy tissues. To improve the low efficacy and toxic side effects of chemotherapies that rely on this passive accumulation, a team of researchers at the Wyss Institute at Harvard University, Boston Children’s Hospital, and Harvard Medical School has developed a new drug delivery platform that uses safe, low-energy ultrasound waves to trigger the dispersal of chemotherapy-containing sustained-release nanoparticles precisely at tumor sites, resulting in a two-fold increase in targeting efficacy and a dramatic reduction in both tumor size and drug-related toxicity in mouse models of breast cancer. This research was recently published in Biomaterials.

    “We essentially have an external activation method that can localize drug delivery anywhere you want it, which is much more effective than just injecting a bunch of nanoparticles,” says co-first author Netanel Korin, Ph.D., former Wyss Technology Development Fellow and current Assistant Professor at the Israel Institute of Technology.

    The key to this new method is the creation of nanoparticle aggregates (NPAs), which are tiny structures consisting of drug-containing nanoparticles surrounded by a supportive matrix, akin to the berries suspended in a blueberry muffin. Like chefs trying to craft the perfect pastry, the researchers experimented with a variety of nanoparticle sizes and nanoparticle-to-matrix ratios to create NPAs that are stable enough to remain intact when injected, but also finely tuned to break apart when disrupted with low-energy ultrasound waves, freeing the nanoparticles that then release their drug payloads over time, like blueberries slowly leaking their juice.

    To test whether the NPAs worked as designed, the team first exposed mouse breast cancer cells to either loose nanoparticles, intact NPAs, or NPAs that had been treated with ultrasound. The ultrasound-treated NPAs and loose nanoparticles both showed greater tumor internalization than the intact NPAs, showing that the ultrasound waves effectively broke up the NPAs to allow the nanoparticles to infiltrate cancer cells.

    Next, the researchers repeated the experiments with nanoparticles containing doxorubicin (a common chemotherapy drug used to treat a variety of cancers) and found that the NPAs resulted in a comparable level of cancer cell death, demonstrating that NPA encapsulation did not negatively impact the efficacy of the drug.

    Finally, to see whether the NPAs performed well compared with loose nanoparticles in vivo, both formulations were injected intravenously into mice with breast cancer tumors. Ultrasound-treated NPAs delivered nearly five times the amount of nanoparticles to the tumor site as intact NPAs, while loose nanoparticles delivered two to three times that amount. When the nanoparticles were loaded with doxorubicin, tumors in mice that received NPAs and ultrasound shrank by nearly half compared with those in mice that received loose nanoparticles. Crucially, by using NPAs, the researchers were able to cut tumor size in half using one-tenth of the dose of doxorubicin usually required, reducing the number of mouse deaths due to drug toxicity from 40% to 0%.

    “Locking nanoparticles up in NPAs permits precise delivery of an army of nanoparticles from each single NPA directly to the tumor in response to ultrasound, and this greatly minimizes the dilution of these nanoparticles in the bloodstream,” says Anne-Laure Papa, Ph.D., co-first author and Postdoctoral Fellow at the Wyss Institute. “Additionally, our ultrasound-triggered NPAs displayed distribution patterns throughout the body similar to the FDA-approved PLGA polymer nanoparticles, so we expect the NPAs to be comparably safe.”

    How ultrasound-sensitive NPAs work: 1. Intact NPAs are introduced into the bloodstream. 2. Ultrasound waves are applied to the site of the tumor. 3. NPAs break apart in response to ultrasound, releasing nanoparticles that deliver their drug payload directly to the tumor. Credit: Wyss Institute at Harvard University

    NPAs were also shown to limit the “burst release” commonly observed in nanoparticle drug delivery, in which a significant number of them break open and release their drug soon after injection, causing an adverse response around the site of injection and reducing the amount of the drug that gets to the tumor. When applied to cancer cells in vitro, loose nanoparticles released 25% of their drug payload within five minutes of being administered, while the nanoparticles contained within intact NPAs released just 1.8% of their drug. When ultrasound was applied, an additional 65% of the drug was released from the NPAs compared with loose nanoparticles, which only released an additional 11%.

    The team says additional research could further improve the performance of ultrasound-sensitive NPAs, making the platform an attractive option for safer, more effective chemotherapy delivery. It could be made even more powerful through combination with other tumor-targeting strategies such as using peptides that home to the tumor microenvironment to further guide cancer drugs to their targets. “We hope that in the future our triggered accumulation technique can be combined with such targeting strategies to produce even more potent treatment effects,” says Papa.

    “This approach offers a novel solution to the pervasive problem of delivering a high concentration of an intravenous drug to a very specific area while sparing the rest of the body,” says senior author and Wyss Founding Director Donald Ingber, M.D., Ph.D., who is also the Judah Folkman Professor of Vascular Biology at Harvard Medical School (HMS) and the Vascular Biology Program at Boston Children’s Hospital, and Professor of Bioengineering at Harvard SEAS. “By using localized ultrasound to selectively deploy sustained-release nanoparticles loaded with high drug concentrations, we have created a non-invasive way to safely and effectively deliver chemotherapy only where and when it’s needed.”

    Mathumai Kanapathipillai, Ph.D., who also co-first authored the paper as a Research Scientist at the Wyss Institute, is currently an Assistant Professor of Mechanical Engineering at University of Michigan-Dearborn. Other contributing authors include Robert Mannix, Ph.D., Oktay Uzun, Ph.D., Christopher Johnson, Deen Bhatta, and Garry Cuneo from the Wyss Institute; and Akiko Mammoto, M.D., Ph.D., Tadanori Mammoto, M.D., Ph.D., and Amanda Jiang from the Vascular Biology Program and Department of Surgery at Boston Children’s Hospital and HMS.

    This research was supported by the US Army Medical Research and Materiel Command under DoD Breast Cancer Innovator Award No. W81XWH-08-1-0659, DoD grant No. W81WXH-10-1-0565, and DoD Breast Cancer Breakthrough Award No. W81XWH-15-1-0305. Opinions, interpretations, conclusions and recommendations are those of the authors and are not necessarily endorsed by the U.S. Army.

    See the full article here .

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    Wyss Institute campus

    The Wyss (pronounced “Veese”) Institute for Biologically Inspired Engineering uses Nature’s design principles to develop bioinspired materials and devices that will transform medicine and create a more sustainable world.

    Working as an alliance among Harvard’s Schools of Medicine, Engineering, and Arts & Sciences, and in partnership with Beth Israel Deaconess Medical Center, Boston Children’s Hospital, Brigham and Women’s Hospital, Dana Farber Cancer Institute, Massachusetts General Hospital, the University of Massachusetts Medical School, Spaulding Rehabilitation Hospital, Tufts University, and Boston University, the Institute crosses disciplinary and institutional barriers to engage in high-risk research that leads to transformative technological breakthroughs.

  • richardmitnick 4:37 am on June 14, 2017 Permalink | Reply
    Tags: , Cancer, ,   

    From COSMOS: “How dissolving cells reveals cancer secrets’ 

    Cosmos Magazine bloc


    13 June 2017
    Anthea Batsakis

    A decellularised mouse mammary gland, stained to show collagen IV, an important molecule in the extracellular matrix. Thomas Cox

    The microscopic structure of tumours has always remained somewhat elusive for biologists. But thanks to a new technique, scientists have, for the first time, seen in three dimensions the “net” that holds our cells in place and gives tissues their shape, known as the extracellular matrix.

    Led by Janine Erler from the University of Copenhagen, where the research took place, this technique may help reveal the architecture of tumours and explain why tumours can grow back in different parts of the body after being removed.

    Until now, studying the extracellular matrix required tissue to be sliced into tiny strips and dropped into a beaker of solution – at best, this technique showed the matrix in two dimensions.

    In research published in Nature Medicine, the scientists instead used blood vessels to transport cell-removing compounds into mouse organ tissue, gently dissolving the cells and hollowing out the organ to leave behind its delicate scaffolding. They call the technique in situ decellurisation of tissue, or ISDoT.

    The fibres of the extracellular matrix, made up of a complex lattice of proteins and carbohydrates secreted from cells, can be seen with far greater clarity without the cells obstructing the view.

    Thomas Cox, one of the authors of the paper, is a cancer cell biologist from the Garvan Institute in Sydney, Australia. “We’ve seen things that we never would have expected and we don’t know exactly what they mean, but that’s all part of the fun,” he says.

    “No has ever seen this before and we’ve got plenty to keep us busy to follow up on.”

    As well as giving physical structure to our tissues, the extracellular matrix also has a powerful influence on cell behaviour.

    When it comes to tumours, the extracellular matrix and cancer cells manipulate one another. Cancer cells, for instance, can create more of the matrix, destroy it and remodel it.

    “This is why our study is important, because it has been shown that as cancer cells change their environment, they’re more able to go on and multiply uncontrollably,” Cox says.

    Using mass spectrometry, Cox and his colleagues identified and catalogued different components of the matrix. Interestingly, they found that the way secondary cancer cells (metastases) remodel the matrix is specific to the organ they’re growing within.

    Queensland University of Technology breast cancer biologist Rik Thompson, who didn’t take part in the study, says the varying structure of the matrix in secondary tumours might be why they’re more difficult to treat.

    “This is exciting in that it provides a robust, validated approach for examining extracellular matrix and already has shown some very new information,” Thompson says.

    “The mass spectroscopy takes the study to a new dimension, with hundreds of proteins identified to vary in the extracellular matrix around cancers compared to the normal tissues.”

    He adds that this new technique will influence his own research on how proportions of breast tissue plays into the risk of breast cancer.

    “This approach would enable us to more comprehensively understand the structure and composition of the extracellular matrix in regions of high versus low mammographic density.”

    See the full article here .

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  • richardmitnick 1:36 pm on June 13, 2017 Permalink | Reply
    Tags: , Cancer, , , The importance of engaging communities in research   

    From Stanford: “The importance of engaging communities in research” 

    Stanford University Name
    Stanford University


    Scope blog

    June 12, 2017

    No image caption or credit.

    Getting help from the community to identify and address health concerns is critical to public-health researchers. That was the message of one of the sessions at the 16th Annual Breast Cancer Conference of the Cancer Prevention Institute of California (CPIC), held earlier this spring.

    The session brought together researchers, clinicians, community advocates, and breast cancer patients and survivors to discuss how unmet community needs can inform research studies in what has come to be known as community-based participatory research (CBPR).

    Panelists emphasized the importance of engaging community advocates as full partners when embarking on a CBPR program and identified these as key things that researchers should do to ensure success:

    Obtain input from the people who are directly impacted by the issues
    Establish equal footing between the researcher and the community in choosing a research topic/program
    Agree on what the outcomes should be (e.g. social/policy changes)
    Empower the community to take action that translates to real transformation once the research study or program is complete

    While the approach needs to be customized for each study, panelists offered some examples of how one might establish or maintain the “buy-in” of a CBPR program:

    Use qualitative data, such as stories from people who have been through the program, which are powerful in demonstrating the value of the study
    Use an integrative approach of policy, advocacy, community outreach and engagement, as well as research to address the big issue.
    Form advisory groups comprised of community members, who are part of the research program, and train them to discuss cancer education and outreach within the community.

    During the session, several researchers provided examples of engaging with various communities in their work. Thu Quach, PhD, an epidemiologist with CPIC, described how fifteen years ago workers with Asian Health Services, a community health center in Oakland, kept hearing local nail salon workers say, “You know, whenever I work in nail salons I breathe a lot of these chemicals and they just don’t make me feel very good.” This led to Quach and other researchers looking into the problem and finding that the chemicals used in nail salons led to health ailments among workers.

    And research was just one piece of an integrative approach of policy, advocacy, community outreach and engagement. While the studies were taking place, Quach explained, the center was simultaneously taking such actions as urging manufacturers of nail polishes to phase out some of the harmful chemicals and training nail salon owners on how to replace those nail polishes with safe alternatives.

    Catherine Thomsen of Zero Breast Cancer described a study looking at early puberty onset and breast cancer. The researchers asked the girls who were part of the study for their opinions and ideas. What questions should be asked? How should the questions be asked? How do they want to communicate with this study? Since these prepubescent girls spent so much time on their mobile phones researchers wound up modifying their interaction around mobile technology.

    Session moderator Judy Luce, MD, a clinical professor at UCSF, also shared an example from earlier in her career at San Francisco General Hospital. A health center was referring a large number of women for mammograms, but many were not showing up for their appointments. Once this health center saw how they compared to other health centers in the area, they took action by assigning a language-appropriate nurse to contact the referred w omen and make sure they knew when their appointment was, how to get there, and essentially guide them through the process. By making these changes, the clinic had the highest mammography rate in the entire system.

    The panelists noted that measuring the impact of a CBPR program presents a challenge since the outcomes, such as reducing the incidence of breast cancer, of any research study may take time to unfold. But, based on these and other examples, this type of research is clearly worth the investment.

    See the full article here .

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    Scope is an award-winning blog founded in 2009 and produced by the Stanford University School of Medicine. If you’re curious about the latest advances in medicine and health and enjoy compelling, fresh and easily digestible news and features, then we’ve got just the thing. We’ve written quite a bit (7,000 posts and counting!), and we’re quite proud of it — so please enjoy.

    Leland and Jane Stanford founded the University to “promote the public welfare by exercising an influence on behalf of humanity and civilization.” Stanford opened its doors in 1891, and more than a century later, it remains dedicated to finding solutions to the great challenges of the day and to preparing our students for leadership in today’s complex world. Stanford, is an American private research university located in Stanford, California on an 8,180-acre (3,310 ha) campus near Palo Alto. Since 1952, more than 54 Stanford faculty, staff, and alumni have won the Nobel Prize, including 19 current faculty members

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  • richardmitnick 2:03 pm on June 9, 2017 Permalink | Reply
    Tags: , Cancer, Cancer Therapeutics CRC (or CTx), , Foetal form of haemoglobin, Haemoglobin, , One step closer to understanding and treating blood cancer, PRMT5 enzyme, Sickle cell anaemia and b-thalassemia   

    From CSIRO: “One step closer to understanding and treating blood cancer” 

    CSIRO bloc

    Commonwealth Scientific and Industrial Research Organisation

    9th June 2017
    Rachael Vorwerk

    Did someone say party? Think again, this confetti-lookalike structure is the PRMT5 enzyme, and if we can find a way to stop it working, then we’ll be one step closer to understanding blood cancers and sickle cell anaemia.

    We’d like to introduce you to an enzyme called PRMT5. Enzymes are the things that make chemical reactions occur and this one is a big deal in cancer (oncology) and blood diseases.

    Like anything, too much of a good thing can turn bad.

    Too much of PRMT5 is often found in many cancers. PRMT5 inactivates another protein called p53, or the ‘guardian of the genome’ as it’s affectionately known. And it’s not called the guardian of the genome for nothing – it forms an integral part of the human body’s surveillance system.


    How does PRMT5 relate to cancer?

    If we could block PRMT5 with a drug (small molecule inhibitor), it would lead to the activation of p53 resulting in the death of the cancer cells.

    For cancer, p53 is especially important because when it is active, many cancers don’t develop. Often when p53 is inactive or mutated in different cancers, (especially blood cancers), it helps cancer develop.

    Put simply:


    PRMT5 and other diseases

    Another important function of PRMT5 is its role in regulating the type of haemoglobin – the protein in our blood that carries oxygen – we make in our red blood cells before and after we are born.

    PRMT5 is a very important enzyme because it’s involved in switching off the foetal form of haemoglobin, which is replaced by adult haemoglobin after we are born.

    Unfortunately, there are diseases such as sickle cell anaemia and b-thalassemia where the adult haemoglobins are mutated.

    However, by using a drug that blocks the activity of PRMT5, it may be possible for patients with sickle cell anaemia and b-thalassemia to remake enough foetal haemoglobin in their bodies to allow them to lead normal lives.

    Where are we up to with this research?

    Cancer Therapeutics CRC (or CTx) has been working on some ground-breaking work in cancer research in this area. They’ve been researching the discovery and development of novel oncology drugs that target PRMT5 for the treatment of solid tumours and blood cancer.

    CTx has just been recognised for their work on the PRMT5 program, with the Australian CRC Association’s (CRCA) Award for Excellence in Innovation. The PRMT5 program that CTx developed was licensed to the global pharmaceutical firm MSD (known as Merck in the US and Canada) in January 2016, in one of the largest ever pre-clinical licensing deals originating from Australian research. We’re proud to say we helped CTx with protein production and the great news is that MSD are continuing to work with us.

    Hopefully soon we’ll be another step closer to figuring out how to stop PRMT5 from working, being that one step closer to understanding common solid tumours and blood cancer.

    Cooperative Research Centres – what they are and why you should know about them

    If you haven’t heard of the Cooperative Research Centres (CRC) Programme, you’re missing out on some innovative work happening around all of Australia. It’s an Australian Government Initiative giving opportunities left, right and centre to businesses with outcome-focused collaborative partnerships. It’s a pretty big deal and opportunity for industry, researchers and the community.

    Want to know more about the great stuff our Cooperative Research Centres are working on? Find out more here!

    See the full article here .

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    CSIRO campus

    CSIRO, the Commonwealth Scientific and Industrial Research Organisation, is Australia’s national science agency and one of the largest and most diverse research agencies in the world.

  • richardmitnick 8:16 pm on June 8, 2017 Permalink | Reply
    Tags: , Cancer, Mammograms: Are we overdiagnosing small tumors?, ,   

    From Yale- “Mammograms: Are we overdiagnosing small tumors?” 

    Yale University bloc

    Yale University

    June 7, 2017

    Renee Gaudette
    (203) 671-8156

    (© stock.adobe.com)

    An analysis of breast cancer data revealed that many small breast cancers have an excellent prognosis because they are inherently slow growing, according to Yale Cancer Center experts. Often, these cancers will not grow large enough to become significant within a patient’s lifetime and subsequently early detection could lead to overdiagnosis, said the reseachers. In contrast, large tumors that cause most breast cancer deaths often grow so quickly that they become intrusive before they can be detected by screening mammography, they note.

    The study, published June 8 in the New England Journal of Medicine, questions the value of breast cancer early detection.

    “Our analysis explains both how mammography causes overdiagnosis and also why it is not more effective in improving outcomes for our patients. More importantly, it questions some of our fundamental beliefs about the value of early detection,” said Donald R. Lannin, M.D., professor of surgery at Yale School of Medicine and lead author on the paper.

    The research team analyzed invasive breast cancers diagnosed between 2001 and 2013 in the Surveillance, Epidemiology, and End Results (SEER) database and divided them into three prognostic groups based on biologic factors: grade, estrogen receptor (ER) status, and progesterone-receptor (PR) status. The three biologic categories were defined as favorable, intermediate, and unfavorable.

    The team, which also included Shiyi Wang, M.D., assistant professor of epidemiology at Yale School of Public Health, then used the expected rate of overdiagnosis of 22% to model the types of breast cancers and patient age ranges that likely account for the majority of overdiagnosis. The results showed that most overdiagnosis occurred in older patients with biologically favorable, slow-growing tumors.

    “Until now, we thought that the lead time, or time until a cancer becomes problematic for a patient, for most breast cancers was about three or four years. This paper shows that lead times vary widely depending on the tumor type. A large portion of aggressive cancers have a lead time of two years or less, whereas another large portion of breast cancers grow so slowly that the lead time is 15 to 20 years,” Lannin explained.

    “It is important that we educate physicians, patients, and the public on the indolent, slow-growing nature of some breast cancers. This knowledge will allow us to individualize treatment options, provide ‘personalized medicine,’ and avoid the major harms of overdiagnosis, which can result in overtreatment and the anxiety and fear that a cancer diagnosis causes,” Lannin said.

    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 8:06 pm on June 8, 2017 Permalink | Reply
    Tags: , Cancer, , Project reveals importance of cancer gene mutation testing,   

    From Vanderbilt: “Project reveals importance of cancer gene mutation testing” 

    Vanderbilt U Bloc

    Vanderbilt University

    Jun. 8, 2017
    Dagny Stuart

    An international genomic data-sharing consortium has analyzed nearly 19,000 patient genomic records and found that testing of patient tumors for relevant gene mutations often provides a roadmap for the use of effective therapies.

    The American Association for Cancer Research (AACR) Genomics Evidence Neoplasia Information Exchange (GENIE) is a multi-phase, multi-year data-sharing project launched in 2015 with eight academic centers. Vanderbilt-Ingram Cancer Center (VICC) is one of the institutions that shared de-identified genomic records from patients treated at the center to determine if genome sequencing can identify clinically useful mutations.

    Mia Levy, M.D., Ph.D., Ingram Professor of Cancer Research and director of Cancer Health Informatics and Strategy, and Christine Micheel, Ph.D., research assistant professor of Medicine and managing editor of My Cancer Genome, led the VICC effort. Thomas Stricker, M.D., Ph.D., Michele LeNoue-Newton, Ph.D., and Lucy Wang also served as authors.

    Mia Levy, M.D., Ph.D.

    One of the criticisms of molecular profiling is the time and financial cost involved in testing all patients since relatively small percentages of patients actually have a mutation that can be treated with a specific therapy. To determine the frequency of important mutations, the AACR Project GENIE group mapped all mutations to variant interpretations merged from other knowledge bases, including My Cancer Genome, OncoKB and Personalized Cancer Therapy.

    The new analysis found that more than 30 percent of the patient samples had mutations that are clinically actionable, meaning patients potentially could be treated with targeted therapies already approved by the U.S. Food and Drug Administration (FDA) or which are being tested in clinical trials.

    These frequencies varied widely across disease, from highly recurrent and druggable mutations in gastrointestinal stromal tumors (GIST) — 66 percent, almost all of which were mutations of KIT and PDGFRA associated with standard-of-care therapies — to tumor types with few actionable alterations, such as renal cell, prostate or pancreatic cancer.

    Breast cancer is the disease with the highest fraction of patients who might benefit from existing investigational targeted therapies, due to frequent mutations of AKT1, ERBB2 and PIK3CA, account­ing for 38 percent of patients.

    The investigators anticipate one of the benefits of GENIE will be an increased power for determining the clinical significance of mutations, particularly new indica­tions for approved drugs, as well as data-driven selection of tumors likely to contain actionable mutations for clinical trials.

    The study was supported by funds from the AACR, Genentech, Boehringer Ingelheim, Pfizer, Eli Lilly, the Howard Hughes Medical Institute, the National Institutes of Health, the National Cancer Institute, the Princess Margaret Cancer Foundation, the Ontario Ministry of Health, Susan G. Komen, the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation, the T.J. Martell Foundation, the Commonwealth Foundation, the Cancer Prevention and Research Institute of Texas, the Dutch Ministry of Health, and the Dutch Cancer Society.

    The other seven institutions that participated in AACR Project GENIE phase 1 are: Dana-Farber Cancer Institute, Boston; Gustave Roussy Cancer Campus, Paris-Villejuif, France; The Netherlands Cancer Institute, Amsterdam, on behalf of the Center for Personalized Cancer Treatment, Utrecht, The Netherlands; Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore; Memorial Sloan Kettering Cancer Center, New York; Princess Margaret Cancer Centre, Toronto; and University of Texas MD Anderson Cancer Center, Houston.

    See the full article here .

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    Commodore Cornelius Vanderbilt was in his 79th year when he decided to make the gift that founded Vanderbilt University in the spring of 1873.

    The $1 million that he gave to endow and build the university was the commodore’s only major philanthropy. Methodist Bishop Holland N. McTyeire of Nashville, husband of Amelia Townsend who was a cousin of the commodore’s young second wife Frank Crawford, went to New York for medical treatment early in 1873 and spent time recovering in the Vanderbilt mansion. He won the commodore’s admiration and support for the project of building a university in the South that would “contribute to strengthening the ties which should exist between all sections of our common country.”

    McTyeire chose the site for the campus, supervised the construction of buildings and personally planted many of the trees that today make Vanderbilt a national arboretum. At the outset, the university consisted of one Main Building (now Kirkland Hall), an astronomical observatory and houses for professors. Landon C. Garland was Vanderbilt’s first chancellor, serving from 1875 to 1893. He advised McTyeire in selecting the faculty, arranged the curriculum and set the policies of the university.

    For the first 40 years of its existence, Vanderbilt was under the auspices of the Methodist Episcopal Church, South. The Vanderbilt Board of Trust severed its ties with the church in June 1914 as a result of a dispute with the bishops over who would appoint university trustees.

    kirkland hallFrom the outset, Vanderbilt met two definitions of a university: It offered work in the liberal arts and sciences beyond the baccalaureate degree and it embraced several professional schools in addition to its college. James H. Kirkland, the longest serving chancellor in university history (1893-1937), followed Chancellor Garland. He guided Vanderbilt to rebuild after a fire in 1905 that consumed the main building, which was renamed in Kirkland’s honor, and all its contents. He also navigated the university through the separation from the Methodist Church. Notable advances in graduate studies were made under the third chancellor, Oliver Cromwell Carmichael (1937-46). He also created the Joint University Library, brought about by a coalition of Vanderbilt, Peabody College and Scarritt College.

    Remarkable continuity has characterized the government of Vanderbilt. The original charter, issued in 1872, was amended in 1873 to make the legal name of the corporation “The Vanderbilt University.” The charter has not been altered since.

    The university is self-governing under a Board of Trust that, since the beginning, has elected its own members and officers. The university’s general government is vested in the Board of Trust. The immediate government of the university is committed to the chancellor, who is elected by the Board of Trust.

    The original Vanderbilt campus consisted of 75 acres. By 1960, the campus had spread to about 260 acres of land. When George Peabody College for Teachers merged with Vanderbilt in 1979, about 53 acres were added.

    wyatt centerVanderbilt’s student enrollment tended to double itself each 25 years during the first century of the university’s history: 307 in the fall of 1875; 754 in 1900; 1,377 in 1925; 3,529 in 1950; 7,034 in 1975. In the fall of 1999 the enrollment was 10,127.

    In the planning of Vanderbilt, the assumption seemed to be that it would be an all-male institution. Yet the board never enacted rules prohibiting women. At least one woman attended Vanderbilt classes every year from 1875 on. Most came to classes by courtesy of professors or as special or irregular (non-degree) students. From 1892 to 1901 women at Vanderbilt gained full legal equality except in one respect — access to dorms. In 1894 the faculty and board allowed women to compete for academic prizes. By 1897, four or five women entered with each freshman class. By 1913 the student body contained 78 women, or just more than 20 percent of the academic enrollment.

    National recognition of the university’s status came in 1949 with election of Vanderbilt to membership in the select Association of American Universities. In the 1950s Vanderbilt began to outgrow its provincial roots and to measure its achievements by national standards under the leadership of Chancellor Harvie Branscomb. By its 90th anniversary in 1963, Vanderbilt for the first time ranked in the top 20 private universities in the United States.

    Vanderbilt continued to excel in research, and the number of university buildings more than doubled under the leadership of Chancellors Alexander Heard (1963-1982) and Joe B. Wyatt (1982-2000), only the fifth and sixth chancellors in Vanderbilt’s long and distinguished history. Heard added three schools (Blair, the Owen Graduate School of Management and Peabody College) to the seven already existing and constructed three dozen buildings. During Wyatt’s tenure, Vanderbilt acquired or built one-third of the campus buildings and made great strides in diversity, volunteerism and technology.

    The university grew and changed significantly under its seventh chancellor, Gordon Gee, who served from 2000 to 2007. Vanderbilt led the country in the rate of growth for academic research funding, which increased to more than $450 million and became one of the most selective undergraduate institutions in the country.

    On March 1, 2008, Nicholas S. Zeppos was named Vanderbilt’s eighth chancellor after serving as interim chancellor beginning Aug. 1, 2007. Prior to that, he spent 2002-2008 as Vanderbilt’s provost, overseeing undergraduate, graduate and professional education programs as well as development, alumni relations and research efforts in liberal arts and sciences, engineering, music, education, business, law and divinity. He first came to Vanderbilt in 1987 as an assistant professor in the law school. In his first five years, Zeppos led the university through the most challenging economic times since the Great Depression, while continuing to attract the best students and faculty from across the country and around the world. Vanderbilt got through the economic crisis notably less scathed than many of its peers and began and remained committed to its much-praised enhanced financial aid policy for all undergraduates during the same timespan. The Martha Rivers Ingram Commons for first-year students opened in 2008 and College Halls, the next phase in the residential education system at Vanderbilt, is on track to open in the fall of 2014. During Zeppos’ first five years, Vanderbilt has drawn robust support from federal funding agencies, and the Medical Center entered into agreements with regional hospitals and health care systems in middle and east Tennessee that will bring Vanderbilt care to patients across the state.

    studentsToday, Vanderbilt University is a private research university of about 6,500 undergraduates and 5,300 graduate and professional students. The university comprises 10 schools, a public policy center and The Freedom Forum First Amendment Center. Vanderbilt offers undergraduate programs in the liberal arts and sciences, engineering, music, education and human development as well as a full range of graduate and professional degrees. The university is consistently ranked as one of the nation’s top 20 universities by publications such as U.S. News & World Report, with several programs and disciplines ranking in the top 10.

    Cutting-edge research and liberal arts, combined with strong ties to a distinguished medical center, creates an invigorating atmosphere where students tailor their education to meet their goals and researchers collaborate to solve complex questions affecting our health, culture and society.

    Vanderbilt, an independent, privately supported university, and the separate, non-profit Vanderbilt University Medical Center share a respected name and enjoy close collaboration through education and research. Together, the number of people employed by these two organizations exceeds that of the largest private employer in the Middle Tennessee region.
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