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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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Promotion of autophagy as a mechanism for radiation sensitization of breast tumor cells.

TL;DR: Studies in the laboratory support the premise that radiosensitization of breast tumor cells by vitamin D or vitamin D analogs is mediated through autophagy, and promotion of autophagic cell death by a vitaminD analog in irradiated breast tumor Cells delays and attenuates the proliferative recovery that may be a preclinical indicator of disease recurrence.
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Potentiation of radiation sensitivity in breast tumor cells by the vitamin D3 analogue, EB 1089, through promotion of autophagy and interference with proliferative recovery

TL;DR: The studies suggest that the effect of EB 1089 treatment on the radiation response is related in part to enhanced promotion of autophagic cell death and in large part to interference with the proliferative recovery that occurs with radiation alone in p53 wild-type breast tumor cells.
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Outcome of early clinical trials of the combination of hydroxychloroquine with chemotherapy in cancer

TL;DR: 5 clinical phase I trials combining hydroxychloroquine with vorinostat, temsirolimus, temozolomide, or bortezomib should provide guidance in the planning and design of future trials to directly determine whether the strategy of autophagy inhibition could prove useful in the treatment of various malignancies.
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Growth arrest and non-apoptotic cell death associated with the suppression of c-myc expression in MCF-7 breast tumor cells following acute exposure to doxorubicin

TL;DR: The down-regulation of c-myc expression may reflect perturbations in regulatory processes contributing to growth arrest in MCF-7 cells exposed to topoisomerase II inhibitors.
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Apoptosis, autophagy, accelerated senescence and reactive oxygen in the response of human breast tumor cells to Adriamycin

TL;DR: These studies suggest that accelerated senescence induced by Adriamycin is similar in cells with wild type p53 and in cells lacking functional p53 with regard to the upregulation of p21(waf1/cip1), down regulation of cdc2 and the involvement of reactive oxygen species.