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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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The lysosome as an imperative regulator of autophagy and cell death.

TL;DR: In this article, a review of Lysosomal reformation, maintenance, and degradation pathways following the involvement of the lysosome in autophagy and cell death, which are related to several pathophysiological conditions observed in humans.
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Autophagy-deficient breast cancer shows early tumor recurrence and escape from dormancy.

TL;DR: Investigation of how autophagy plays a role in accelerating or delaying recurrence of neu-overexpressing mouse mammary carcinoma following adriamycin (ADR) treatment, and in affecting response to immunotherapy suggests cell-intrinsicautophagy delays tumor relapse, in part, by inhibiting the formation of polyploid-like tumor dormancy.
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Colchicine site inhibitors of microtubule integrity as vascular disrupting agents

TL;DR: A more comprehensive understanding of tumor compensatory mechanisms and potential combination strategies with anti‐angiogenic agents suggest that vascular targeting therapy may be a fruitful direction for the further development of this class of drugs as anticancer agents.
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Effect of the vitamin D3 analog ILX 23-7553 on apoptosis and sensitivity to fractionated radiation in breast tumor cells and normal human fibroblasts

TL;DR: ILX 23-7553 enhanced the antiproliferative and apoptotic effects of fractionated ionizing radiation in MCF-7 breast cancer cells and appeared to be selective in that similar responses were not observed in a model of normal human fibroblasts.
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The Autophagic Response to Radiation: Relevance for Radiation Sensitization in Cancer Therapy

TL;DR: Concerns are raised as to whether chloroquine and hydroxychloroquine, the agents currently in use, have the capacity to suppress autophagy when administered systemically at tolerable doses and any agent that actually has the appropriate pharmacokinetic profile to function as a systemic Autophagy inhibitor may collaterally disrupt the homeostatic function of autophagic in normal cells.