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Jayashree Karar

Researcher at University of Pennsylvania

Publications -  21
Citations -  1697

Jayashree Karar is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: PI3K/AKT/mTOR pathway & Kinase. The author has an hindex of 17, co-authored 20 publications receiving 1348 citations. Previous affiliations of Jayashree Karar include Wistar Institute & Savitribai Phule Pune University.

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PI3K/AKT/mTOR Pathway in Angiogenesis

TL;DR: The PI3K pathway plays an important role in regulating angiogenesis both in normal tissues and in cancers, and numerous inhibitors targeting the PI3k/AKT/mTOR pathway have been developed, and these agents have been shown to decrease VEGF secretion and angiynthesis.
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Germline Mutation of Bap1 Accelerates Development of Asbestos-Induced Malignant Mesothelioma

TL;DR: Unbiased genetic findings indicate that BAP1 mutation carriers are predisposed to the tumorigenic effects of asbestos and suggest that high penetrance of mesothelioma requires such environmental exposure.
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Modulating the tumor microenvironment to increase radiation responsiveness.

TL;DR: The challenge remains to obtain clinical data from patients showing that modulation of the TME is an important mechanism by which biological agents can radiosensitize tumors and then to utilize this information to optimize therapy.
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Inhibition of autophagy as a strategy to augment radiosensitization by the dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235.

TL;DR: It is concluded that NVP-BEZ235 radiosensitizes cells and induces autophagy by apparently distinct mechanisms, and the data offer a rationale for combining N VP-BEz235 along with an Autophagy inhibitor and radiation in future clinical trials.
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Anti-tumorigenic effects of Type 1 interferon are subdued by integrated stress responses.

TL;DR: Hypoxia can elicit effects of phosphorylation-dependent degradation of the IFNAR1 chain of the Type 1 interferon (IFN) receptor in a PERK-dependent manner and enables multiple cellular components of tumor tissue to evade the direct and indirect anti-tumorigenic effects of Type 1 IFN.