7 thoughts on “JC 9.3.2016: General”

  1. TOPI

    NATURE | LETTER

    Mutant Kras copy number defines metabolic reprogramming and therapeutic susceptibilities
    Emma M. Kerr, Edoardo Gaude, Frances K. Turrell, Christian Frezza & Carla P. Martins
    Nature 531, 110–113 (03 March 2016) doi:10.1038/nature16967

    Click to access nature16967.pdf

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  2. High-fat diet enhances stemness and tumorigenicity of intestinal progenitors
    Nature 531, 53–58 (03 March 2016)

    Semir Beyaz, Miyeko D. Mana, Jatin Roper, Dmitriy Kedrin, Assieh Saadatpour, Sue-Jean Hong, Khristian E. Bauer-Rowe, Michael E. Xifaras, Adam Akkad, Erika Arias, Luca Pinello, Yarden Katz, Shweta Shinagare, Monther Abu-Remaileh, Maria M. Mihaylova, Dudley W. Lamming, Rizkullah Dogum, Guoji Guo, George W. Bell, Martin Selig, G. Petur Nielsen, Nitin Gupta, Cristina R. Ferrone, Vikram Deshpande, Guo-Cheng Yuan et al.

    http://www.nature.com/nature/journal/v531/n7592/full/nature17173.html

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  3. http://www.nature.com/onc/journal/v35/n9/full/onc2015151a.html

    Review

    Oncogene (2016) 35, 1073–1079; doi:10.1038/onc.2015.151; published online 18 May 2015

    Opportunities and challenges provided by crosstalk between signalling pathways in cancer

    A Prahallad1 and R Bernards1

    1Division of Molecular Carcinogenesis and Cancer Genomics Netherlands, The Netherlands Cancer Institute, Amsterdam, Netherlands

    Received 13 January 2015; Revised 4 March 2015; Accepted 4 March 2015
    Advance online publication 18 May 2015

    Abstract
    During evolution, connections between the major signalling pathways were established to provide cells with an ability to deal with perturbations of homeostasis. However, these feedback and crosstalk mechanisms can become a liability in the treatment of cancer, as the inhibition of one cancer-relevant signalling pathway can lead to the activation of a secondary survival pathway that interferes with cancer drug efficacy. In this review, we discuss connections between signalling pathways in relation to cancer therapy and we evaluate the use of genetic approaches to identify pathway crosstalk. We also discuss how insight into connections between signalling pathways can be exploited to design powerful synthetic lethal drug combination therapies for the treatment of cancer.

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  4. Cancer Res. 2016 Mar 1;76(5):1122-34. doi: 10.1158/0008-5472.CAN-15-1962. Epub 2015 Dec 23.
    PDLIM1 Stabilizes the E-Cadherin/β-Catenin Complex to Prevent Epithelial-Mesenchymal Transition and Metastatic Potential of Colorectal Cancer Cells.
    Chen HN1, Yuan K1, Xie N1, Wang K1, Huang Z1, Chen Y1, Dou Q1, Wu M2, Nice EC3, Zhou ZG4, Huang C4.

    http://www.ncbi.nlm.nih.gov/pubmed/26701804

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