C
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
The heat shock proteins as targets for radiosensitization and chemosensitization in cancer
TL;DR: Attempts to target these proteins, particularly the small HSPs, in developing potent radiation and chemotherapy sensitizers, are focused on, as well as proposed mechanisms for this sensitization effect.
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PERK-dependent regulation of HSP70 expression and the regulation of autophagy
Margaret A. Park,David T. Curiel,Constantinos Koumenis,Martin R. Graf,Ching-Shih Chen,Paul B. Fisher,Steven Grant,Paul Dent +7 more
TL;DR: The mechanism(s) by which OSU-03012 kills transformed cells is defined and PERK signaling promotes autophagy, which is causally linked to lysosomal dysfunction, cathepsin activation and cell death, but in parallel,PERK signaling acts to suppress autophagic and lysOSomal dysfunction by increasing the expression of HSP70.
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Activation of p38α stress-activated protein kinase drives the formation of the pre-metastatic niche in the lungs.
Jun Gui,Farima Zahedi,Angelica Ortiz,Christina Cho,Kanstantsin V. Katlinski,Kevin Alicea-Torres,Jinyang Li,Leslie Todd,Hongru Zhang,Daniel P. Beiting,Cindy Sander,John M. Kirkwood,Bryan E. Snow,Andrew Wakeham,Tak W. Mak,J. Alan Diehl,Constantinos Koumenis,Sandra Ryeom,Ben Z. Stanger,Ellen Puré,Dmitry I. Gabrilovich,Serge Y. Fuchs +21 more
TL;DR: It is reported that TDFs-induced activation of the p38α kinase in lung fibroblasts plays a critical role in the formation of a pre-metastatic niche in the lungs and subsequent pulmonary metastases.
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Signaling through alternative Integrated Stress Response pathways compensates for GCN2 loss in a mouse model of soft tissue sarcoma
TL;DR: It is demonstrated in a genetically engineered mouse model of soft tissue sarcoma that loss of GCN2 has no effect on tumor growth or animal survival, and these results have important implications for the development and testing of small molecule inhibitors of ISR kinases as cancer therapeutics.
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A Novel Mouse Model to Study Image-Guided, Radiation-Induced Intestinal Injury and Preclinical Screening of Radioprotectors.
Ioannis I. Verginadis,Rahul Kanade,Brett Bell,Sravya Koduri,Edgar Ben-Josef,Constantinos Koumenis +5 more
TL;DR: The model employs a radiopaque marker implanted into the surface of the mouse jejunum, serving as a fiducial marker for precise radiation targeting, and shows significant decreases in both local and systemic inflammatory cytokine levels and in fibrosis, suggesting it is an effective radioprotector of the intestine.