PI3K p110δ uniquely promotes gain-of-function Shp2-induced GM-CSF hypersensitivity in a model of JMML-Reference-Cited by-同舟云学术

PI3K p110δ uniquely promotes gain-of-function Shp2-induced GM-CSF hypersensitivity in a model of JMML

Published:2014-05-01 Issue:18 Volume:123 Page:2838-2842
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

Goodwin Charles B¹²,Li Xing Jun¹³,Mali Raghuveer S.¹,Chan Gordon⁴,Kang Michelle⁵,Liu Ziyue⁶,Vanhaesebroeck Bart⁷^ORCID,Neel Benjamin G.⁴,Loh Mignon L.⁵,Lannutti Brian J.⁸,Kapur Reuben¹²³⁹,Chan Rebecca J.¹²³

Affiliation:

1. Herman B Wells Center for Pediatric Research,

2. Department of Medical & Molecular Genetics, and

3. Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN;

4. Princess Margaret Cancer Center, University Health Network, Toronto, Ontario, Canada;

5. Department of Pediatrics, Division of Hematology Oncology, University of California, San Francisco, CA;

6. Department of Medicine, Division of Biostatistics, Indiana University School of Medicine, Indianapolis, IN;

7. Centre for Cell Signalling, Institute of Cancer, Queen Mary University of London, London, United Kingdom;

8. Acerta Pharma, San Carlos, CA; and

9. Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN

Abstract

Key Points Compared with ubiquitously expressed PI3K p110α, genetic inhibition of PI3K p110δ uniquely normalizes mutant Shp2-induced GM-CSF hypersensitivity. Potent pharmacologic inhibitors of PI3K p110δ cooperate with MEK inhibition to reduce mutant Shp2-induced hyperproliferation.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

http://ashpublications.org/blood/article-pdf/123/18/2838/1376971/2838.pdf

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4. A selective inhibitor of the p110delta isoform of PI 3-kinase inhibits AML cell proliferation and survival and increases the cytotoxic effects of VP16.;Billottet;Oncogene,2006

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