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Constantinos Koumenis

Researcher at University of Pennsylvania

Publications -  156
Citations -  15751

Constantinos Koumenis is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Unfolded protein response & Tumor microenvironment. The author has an hindex of 52, co-authored 129 publications receiving 13837 citations. Previous affiliations of Constantinos Koumenis include Wake Forest University & Wake Forest Baptist Medical Center.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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ER stress‐regulated translation increases tolerance to extreme hypoxia and promotes tumor growth

TL;DR: It is demonstrated that cells cultured under hypoxic/anoxic conditions and transformed cells in hypoxic areas of tumors activate a translational control program known as the integrated stress response (ISR), which adapts cells to endoplasmic reticulum (ER) stress and suggests that this pathway is an attractive target for antitumor modalities.
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Regulation of protein synthesis by hypoxia via activation of the endoplasmic reticulum kinase perk and phosphorylation of the translation initiation factor eif2alpha

TL;DR: Results indicate that adaptation of cells to hypoxic stress requires activation of PERK and phosphorylation of eIF2α and suggest that the mechanism of hypoxia-induced translational attenuation may be linked to ER stress and the unfolded-protein response.
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The GCN2-ATF4 pathway is critical for tumour cell survival and proliferation in response to nutrient deprivation

TL;DR: It is concluded that the GCN2‐eIF2α‐ATF4 pathway is critical for maintaining metabolic homeostasis in tumour cells, making it a novel and attractive target for anti‐tumour approaches.
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Targeting ER stress–induced autophagy overcomes BRAF inhibitor resistance in melanoma

TL;DR: Using tumor biopsies from BRAF(V600E) melanoma patients treated either with BRAFi or with combined BRAF and MEK inhibition, it is found that BRAFi-resistant tumors had increased levels of autophagy compared with baseline and a rationale for combination approaches targeting this resistance pathway is provided.