Sandra Galoforo
Beaumont Hospital
37 Papers
418 Citations
Sandra Galoforo is an academic researcher from Beaumont Hospital. The author has contributed to research in topics: Transfection & Gene expression. The author has an hindex of 17, co-authored 34 publications. Previous affiliations of Sandra Galoforo include Beaumont Health.
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Papers
Glucose deprivation-induced oxidative stress in human tumor cells. A fundamental defect in metabolism?
TL;DR: It is proposed that intracellular oxidation/reduction reactions involving hydroperoxides and thiols may provide a mechanistic link between metabolism, signal transduction, and gene expression in these human tumor cells.
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Glucose deprivation-induced cytotoxicity in drug resistant human breast carcinoma MCF-7/ADR cells: role of c-myc and bcl-2 in apoptotic cell death
Yong J. Lee,Sandra Galoforo,Christine M. Berns,William P. Tong,Hyeong Reh Choi Kim,Peter M. Corry +5 more
TL;DR: Results indicate that c-myc expression is a necessary component of glucose-free medium induced apoptosis and bcl-2 prevents apoptotic death induced by c- myc.
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Adenoviral transduction of a cytosine deaminase/thymidine kinase fusion gene into prostate carcinoma cells enhances prodrug and radiation sensitivity.
TL;DR: Prostate tumor cells (PC‐3) were transduced with defective, recombinant adenovirus containing a fusion gene encoding the Escherichia coli cytosine deaminase and herpes simplex virus type‐1 thymidine kinase under the control of a cytomegalovirus promoter to sensitized to killing by the normally innocuous prodrugs.
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Thermal response in murine L929 cells lacking αB-crystallin expression and αB-crystallin expressing L929 transfectants
Robert V. Blackburn,Sandra Galoforo,Christine M. Berns,Mark E. Ireland,Joong M. Cho,Peter M. Corry,Yong J. Lee +6 more
TL;DR: Though expression of αB-crystallin is not requisite for the development of thermotolerance in L929 cells, overexpression of transfected β-Crystallin can contribute to increased thermoresistance.
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Dominant-negative Jun N-terminal protein kinase (JNK-1) inhibits metabolic oxidative stress during glucose deprivation in a human breast carcinoma cell line.
Yong J. Lee,Sandra Galoforo,Julia E. Sim,Lisa A. Ridnour,Jinah Choi,Henry Jay Forman,Peter M. Corry,Douglas R. Spitz +7 more
TL;DR: Results show that expression of a dominant negative JNK1 protein was capable of suppressing persistent JNK activation as well as oxidative stress and cytotoxicity caused by glucose deprivation in MCF-7/ADR, and support the hypothesis that JNK signaling pathways may control the expression of proteins contributing to cell death mediated by metabolic oxidative stress during glucose deprivation.
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