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The phosphoinositide 3-kinase pathway and therapy resistance in cancer

Content Provider	Semantic Scholar
Author	Brown, Kristin K. Toker, A. C.
Copyright Year	2015
Abstract	The phosphoinositide 3-kinase (PI3K)/Akt/mechanistic target of rapamycin (mTOR) signaling network is a master regulator of processes that contribute to tumorigenesis and tumor maintenance. The PI3K pathway also plays a critical role in driving resistance to diverse anti-cancer therapies. This review article focuses on mechanisms by which the PI3K pathway contributes to therapy resistance in cancer, and highlights potential combination therapy strategies to circumvent resistance driven by PI3K signaling. In addition, resistance mechanisms that limit the clinical efficacy of small molecule inhibitors of the PI3K pathway are discussed.
Starting Page	61
Ending Page	70
Page Count	10
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://f1000researchdata.s3.amazonaws.com/f1000reports/files/9002/7/13/article.pdf
Alternate Webpage(s)	https://dash.harvard.edu/bitstream/handle/1/14351274/4335789.pdf?isAllowed=y&sequence=1
Alternate Webpage(s)	https://dash.harvard.edu/bitstream/handle/1/14351274/4335789.pdf?sequence=1
Alternate Webpage(s)	http://f1000.com/prime/reports/b/7/13/pdf
PubMed reference number	25750731
Alternate Webpage(s)	https://doi.org/10.12703/P7-13
DOI	10.12703/p7-13
Journal	F1000prime reports
Volume Number	7
Language	English
Access Restriction	Open
Subject Keyword	1-Phosphatidylinositol 3-Kinase 1-Phosphatidylinositol-4,5-bisphosphate phosphodiesterase Carcinogenesis Combined Modality Therapy Neoplasms Phosphatidylinositols Sirolimus Small Molecule cancer therapy
Content Type	Text
Resource Type	Article

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Sequential application of a cytotoxic nanoparticle and a PI3K inhibitor enhances antitumor efficacy.

Tyrosine phosphorylation of B-cell adaptor for phosphoinositide 3-kinase is required for Akt activation in response to CD19 engagement.

The phosphoinositide 3-kinase inhibitor LY294002 enhances cardiac myocyte contractility via a direct inhibition of Ik,slow currents.

Identification of novel effectors of invasive cell growth downstream of phosphoinositide 3-kinase.

LY294002 and LY303511 sensitize tumor cells to drug-induced apoptosis via intracellular hydrogen peroxide production independent of the phosphoinositide 3-kinase-Akt pathway.

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The phosphoinositide 3-kinase pathway and therapy resistance in cancer

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Sequential application of a cytotoxic nanoparticle and a PI3K inhibitor enhances antitumor efficacy.

Tyrosine phosphorylation of B-cell adaptor for phosphoinositide 3-kinase is required for Akt activation in response to CD19 engagement.

The phosphoinositide 3-kinase inhibitor LY294002 enhances cardiac myocyte contractility via a direct inhibition of Ik,slow currents.

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