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Phillip A. Dennis

Researcher at Johns Hopkins University School of Medicine

Publications -  100
Citations -  13820

Phillip A. Dennis is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Protein kinase B & PI3K/AKT/mTOR pathway. The author has an hindex of 46, co-authored 100 publications receiving 12997 citations. Previous affiliations of Phillip A. Dennis include National Institutes of Health & Memorial Sloan Kettering Cancer Center.

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Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes

Daniel J. Klionsky, +235 more
- 16 Feb 2008 - 
TL;DR: A set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes are presented.
Journal Article

Akt/Protein Kinase B Is Constitutively Active in Non-Small Cell Lung Cancer Cells and Promotes Cellular Survival and Resistance to Chemotherapy and Radiation

TL;DR: Akt/PKB is identified as a constitutively active kinase that promotes survival of NSCLC cells and modulation of Akt/P KB activity by pharmacological or genetic approaches alters the cellular responsiveness to therapeutic modalities typically used to treat patients withNSCLC.
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Targeting the PI3K/Akt/mTOR pathway: effective combinations and clinical considerations

TL;DR: This review will provide an update on the clinical progress of various agents that target the PI3K/Akt/mTOR pathway and discuss strategies to combine these pathway inhibitors with conventional chemotherapy, radiotherapy, as well as newer targeted agents.
Journal ArticleDOI

PTEN loss in the continuum of common cancers, rare syndromes and mouse models

TL;DR: StudyingPTEN in the continuum of rare syndromes, common cancers and mouse models provides insight into the role of PTEN in tumorigenesis and will inform targeted drug development.
Journal Article

Constitutive and inducible Akt activity promotes resistance to chemotherapy, trastuzumab, or tamoxifen in breast cancer cells.

TL;DR: It is shown that endogenous Akt activity promotes breast cancer cell survival and therapeutic resistance, and that induction of Akt by chemotherapy, trastuzumab, or tamoxifen might be an early compensatory mechanism that could be exploited to increase the efficacy of these therapies.