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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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Effects of Radiation Quality and Oxygen on Clustered DNA Lesions and Cell Death

TL;DR: The Monte Carlo Damage Simulation (MCDS) is extended to account for reductions in the initial lesion yield arising from enhanced chemical repair of DNA radicals under hypoxic conditions, and the kinetic energy range and types of particles considered in the MCDS have been expanded to include charged particles up to and including 56Fe ions.
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The chemopreventive agent curcumin is a potent radiosensitizer of human cervical tumor cells via increased reactive oxygen species production and overactivation of the mitogen-activated protein kinase pathway.

TL;DR: A novel mechanism for curcumin-mediated radiosensitization involving increased ROS and ERK1/2 activation is suggested andCurcumin application (either systemically or topically) may be an effective radiation modifying modality in the treatment of cervical cancer.
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Control of the hypoxic response through regulation of mRNA translation.

TL;DR: Inhibition of mRNA translation is hypothesized to affect the cellular tolerance to hypoxia in part by promoting energy homeostasis, however, regulation of translation also results in a specific increase in the synthesis of a subset of Hypoxia induced proteins.
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Inhibition of fatty acid synthase induces endoplasmic reticulum stress in tumor cells.

TL;DR: The results provide the first evidence that FAS inhibitors induce ER stress and establish an important mechanistic link between FAS activity and ER function.
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Inactivation of Interferon Receptor Promotes the Establishment of Immune Privileged Tumor Microenvironment

TL;DR: Downregulation of IFNAR1 in tumor stroma stimulated CRC development and growth, played a key role in formation of the immune-privileged niche, and predicted poor prognosis in human CRC patients, providing the rationale for upregulating IFnAR1 to improve anti-cancer therapies.