38,004 research outputs found

    Waging war against pancreatic cancer: an interview with David Tuveson

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    David Tuveson, Director of the Cancer Center at Cold Spring Harbor Laboratory, is a clinician-scientist with a longstanding interest in understanding and treating pancreatic cancer. Since developing the first mouse model of pancreatic cancer in 2002, the Tuveson lab has made a series of discoveries that shed light on the molecular drivers of this disease and provide promising therapeutic avenues for a malignancy that is notoriously challenging to treat. In collaboration with Hans Clevers, David developed the first pancreatic cancer organoids, which revolutionized the field by providing a powerful model system for basic discoveries and advancement of personalized medicine. Here, David talks to Ross Cagan about his path from chemistry student to world-renowned oncologist, highlighting how his colleagues, mentors and patient interactions shaped his research interests and unique approach to scientific discovery. As well as discussing the story behind some of his breakthroughs, he provides tips on running a lab and succeeding in or outside academia

    Waging war against pancreatic cancer: an interview with David Tuveson

    No full text
    David Tuveson, Director of the Cancer Center at Cold Spring Harbor Laboratory, is a clinician-scientist with a longstanding interest in understanding and treating pancreatic cancer. Since developing the first mouse model of pancreatic cancer in 2002, the Tuveson lab has made a series of discoveries that shed light on the molecular drivers of this disease and provide promising therapeutic avenues for a malignancy that is notoriously challenging to treat. In collaboration with Hans Clevers, David developed the first pancreatic cancer organoids, which revolutionized the field by providing a powerful model system for basic discoveries and advancement of personalized medicine. Here, David talks to Ross Cagan about his path from chemistry student to world-renowned oncologist, highlighting how his colleagues, mentors and patient interactions shaped his research interests and unique approach to scientific discovery. As well as discussing the story behind some of his breakthroughs, he provides tips on running a lab and succeeding in or outside academia.</jats:p

    Interview with Dr. Tuveson from <i>nab</i>-Paclitaxel Potentiates Gemcitabine Activity by Reducing Cytidine Deaminase Levels in a Mouse Model of Pancreatic Cancer

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    mp3 file (10 MB). In the March edition of the Cancer Discovery podcast, Executive Editor Mark Landis talks with David A. Tuveson about his paper, which provides mechanistic insight into the clinical cooperation observed between gemcitabine and nab-paclitaxel in the treatment of pancreatic cancer.</p

    The RAS and YAP1 dance, who is leading?

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    The Hippo‐signaling effector YAP1 was recently found to compensate for oncogenic RAS in certain neoplasms, suggesting so far unanticipated molecular interplays between these major signaling routes. A new study in this issue of The EMBO Journal details KRAS‐dependent control of YAP1 stability as well as positive feedback regulation via the RAS/YAP1/EGFR‐ligand axis as novel molecular mechanisms that could become exploitable for therapeutic strategies

    The David W. Fentress Family Letters, 1856-1969

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    Transcript of a letter by an unidentified author to David Fentress regarding sharing federal newspapers and the banning of federal newspapers in some areas. The author passes on the news of the war including the destruction of the Federal merchantmen by the Confederate fleet. He passes along world news: Russia preparing to go to War with Europe and how that could negatively affect the Confederacy. There is also speculation on the future of the war

    Stromal biology and therapy in pancreatic cancer: a changing paradigm

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    Pancreatic ductal adenocarcinoma (PDA) exhibits one of the poorest prognosis of all solid tumours and poses an unsolved problem in cancer medicine. Despite the recent success of two combination chemotherapies for palliative patients, the modest survival benefits are often traded against significant side effects and a compromised quality of life. Although the molecular events underlying the initiation and progression of PDA have been intensively studied and are increasingly understood, the reasons for the poor therapeutic response are hardly apprehended. One leading hypothesis over the last few years has been that the pronounced tumour microenvironment in PDA not only promotes carcinogenesis and tumour progression but also mediates therapeutic resistance. To this end, targeting of various stromal components and pathways was considered a promising strategy to biochemically and biophysically enhance therapeutic response. However, none of the efforts have yet led to efficacious and approved therapies in patients. Additionally, recent data have shown that tumour-associated fibroblasts may restrain rather than promote tumour growth, reinforcing the need to critically revisit the complexity and complicity of the tumour-stroma with translational implications for future therapy and clinical trial design

    Portrait of author David Foster at the National Library of Australia, Canberra, 8 June 2011 /

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    Title from acquisitions documentation.; Part of the collection: Portraits of author David Foster at the National Library of Australia, Canberra, 8 June 2011.; Acquired in digital format; access copy available online.; Mode of access: Online.; Photographed by a staff member of the National Library of Australia

    Author David Foster with academic Jeff Doyle at the National Library of Australia, Canberra, 8 June 2011 /

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    Title from acquisitions documentation.; Part of the collection: Portraits of author David Foster at the National Library of Australia, Canberra, 8 June 2011.; Acquired in digital format; access copy available online.; Mode of access: Online.; Photographed by a staff member of the National Library of Australia
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