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      The PI3K pathway in human disease

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          Abstract

          Phosphoinositide 3-kinase (PI3K) activity is stimulated by diverse oncogenes and growth factor receptors, and elevated PI3K signaling is considered a hallmark of cancer. Many PI3K pathway-targeted therapies have been tested in oncology trials, resulting in regulatory approval of one isoform-selective inhibitor (idelalisib) for treatment of certain blood cancers, and a variety of other agents at different stages of development. In parallel to PI3K research by cancer biologists, investigations in other fields have uncovered exciting and often unpredicted roles for PI3K catalytic and regulatory subunits in normal cell function and in disease. Many of these functions impinge upon oncology by influencing the efficacy and toxicity of PI3K-targeted therapies. Here we provide a perspective on the roles of class I PI3Ks in the regulation of cellular metabolism and in immune system functions, two topics closely intertwined with cancer biology. We also discuss recent progress developing PI3K-targeted therapies for treatment of cancer and other diseases.

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          Author and article information

          Journal
          0413066
          2830
          Cell
          Cell
          Cell
          0092-8674
          1097-4172
          15 August 2017
          10 August 2017
          10 August 2018
          : 170
          : 4
          : 605-635
          Affiliations
          [1 ]Department of Molecular Biology & Biochemistry, University of California, Irvine, Irvine, CA 92697-3900 USA
          [2 ]Meyer Cancer Center, Weill Cornell Medical College, 413 E. 69 th Street, New York, NY 10021
          [3 ]Oncology R&D Group, Pfizer Worldwide Research and Development, 10646/CB4 Science Center Drive, San Diego, CA 92121
          Author notes
          [* ]Address correspondence to: David A. Fruman, University of California, Irvine, 3242 McGaugh Hall, Irvine, CA 92697-3900; phone: (949) 824-1947; fax: (949) 824-8551; dfruman@ 123456uci.edu
          Article
          PMC5726441 PMC5726441 5726441 nihpa895027
          10.1016/j.cell.2017.07.029
          5726441
          28802037
          81db4488-64cd-44dd-ac1d-9c7b845bd8a3
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