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David A. Gewirtz

Researcher at Virginia Commonwealth University

Publications -  182
Citations -  22854

David A. Gewirtz is an academic researcher from Virginia Commonwealth University. The author has contributed to research in topics: Autophagy & Cancer. The author has an hindex of 47, co-authored 162 publications receiving 18755 citations. Previous affiliations of David A. Gewirtz include VCU Medical Center.

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A mouse model of radiation-induced cardiomyopathy

TL;DR: A systematic study of XRT-induced cardiomyopathy in the mouse and the incidence and pathophysiology remains poorly described due to a lack of prospective data and a latency period that exceeds the follow-up duration of most clinical studies.
Journal Article

Characterization of a K562 Multidrug-resistant Cell Line

TL;DR: Transport studies indicate reduced intracellular accumulation and retention of daunorubicin in the K562-R cells as compared to the parent cell line, and suggest the presence of distinct cellular pools composed of both rapidly and slowly exchanging drug, with the rapidly exchanging pool being more pronounced in the resistant line.
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Potentiation of cell killing by fractionated radiation and suppression of proliferative recovery in MCF-7 breast tumor cells by the Vitamin D3 analog EB 1089.

TL;DR: Data indicate that EB 1089 (and 1alpha, 25 dihydroxycholecalciferol or its analogs) could selectively enhance breast tumor cell sensitivity to radiation through the promotion of cell death, in part through the generation of ceramide and the suppression of polo-like kinase.
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Antagonism between tamoxifen and doxorubicin in the MCF-7 human breast tumor cell line

TL;DR: Analysis of the influence of tamoxifen on growth inhibition by doxorubicin in the MCF-7 breast tumor cell line in vitro provided clear evidence of antagonism between these agents.
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Radiosensitization of MDA-MB-231 breast tumor cells by adenovirus-mediated overexpression of a fragment of the XRCC4 protein

TL;DR: Clonogenic survival assays showed that the adenovirus expressing the truncated XRCC4 protein sensitizes MDA-MB-231 breast tumor cells to ionizing radiation, presumably through interference with the functional activity of ligase IV, leading to inhibition of the final ligation step in end joining.