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1 August 2013
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Curry and colleagues made the surprising observation that two adjacent tumor types with either low or high AKT activity can develop in Pten-null lungs. Heterogeneous AKT activation was cell autonomous and associated with differential expression of ectonucleoside triphosphate diphospho-hydrolase 5 (ENTPD5), a UDPase that promotes receptor tyrosine kinase folding in the endoplasmic reticulum. Knockdown of ENTPD5 led to a reduction in levels of insulin growth factor receptor Iβ (IGFIRβ), an upstream activator of AKT. In human non–small cell lung cancers (NSCLC), AKT phosphorylation was directly correlated with ENTPD5 expression, but not always with loss of PTEN expression. Together, these findings suggest that PTEN loss may not be sufficient to activate AKT and may not be an appropriate biomarker of PI3K/AKT activation or response to PI3K/AKT-targeted therapies. For details, please see the article by Curry and colleagues on page 908. - PDF Icon PDF LinkTable of Contents
ISSN 2159-8274
EISSN 2159-8290
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Metabolic and Functional Genomic Studies Identify Deoxythymidylate Kinase as a Target in LKB1-Mutant Lung Cancer
Yan Liu; Kevin Marks; Glenn S. Cowley; Julian Carretero; Qingsong Liu; Thomas J.F. Nieland; Chunxiao Xu; Travis J. Cohoon; Peng Gao; Yong Zhang; Zhao Chen; Abigail B. Altabef; Jeremy H. Tchaicha; Xiaoxu Wang; Sung Choe; Edward M. Driggers; Jianming Zhang; Sean T. Bailey; Norman E. Sharpless; D. Neil Hayes; Nirali M. Patel; Pasi A. Janne; Nabeel Bardeesy; Jeffrey A. Engelman; Brendan D. Manning; Reuben J. Shaw; John M. Asara; Ralph Scully; Alec Kimmelman; Lauren A. Byers; Don L. Gibbons; Ignacio I. Wistuba; John V. Heymach; David J. Kwiatkowski; William Y. Kim; Andrew L. Kung; Nathanael S. Gray; David E. Root; Lewis C. Cantley; Kwok-Kin Wong
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