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Mala Shanmugam

Researcher at Emory University

Publications -  36
Citations -  5464

Mala Shanmugam is an academic researcher from Emory University. The author has contributed to research in topics: Glucose transporter & Multiple myeloma. The author has an hindex of 14, co-authored 29 publications receiving 4181 citations. Previous affiliations of Mala Shanmugam include Northwestern University & Children's Memorial Hospital.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Glucose transporters in cancer metabolism.

TL;DR: Tumor cells exhibit elevated levels of glucose uptake, a phenomenon that has been capitalized upon for the prognostic and diagnostic imaging of a wide range of cancers using radio-labeled glucose analogs, but researchers have not yet been able to target glucose entry in a tumor cell-specific manner for therapy.
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Multiple myeloma exhibits novel dependence on GLUT4, GLUT8, and GLUT11: implications for glucose transporter-directed therapy

TL;DR: Critical roles for novel GLUT family members are revealed and a therapeutic strategy entailing selective GLUT inhibition to specifically target aberrant glucose metabolism in cancer is highlighted.
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Cancer Metabolism and the Evasion of Apoptotic Cell Death.

TL;DR: This review attempts to dissect a causal relationship between two cancer hallmarks, i.e., deregulated cellular energetics and the evasion of programmed cell death with primary focus on the intrinsic pathway of apoptosis.
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Targeting glutamine metabolism in multiple myeloma enhances BIM binding to BCL-2 eliciting synthetic lethality to venetoclax.

TL;DR: Investigation revealed that cells surviving glutamine withdrawal in particular, enhance expression and binding of BIM to BCL-2, consequently sensitizing these cells to the BH3 mimetic venetoclax, revealing a potent therapeutic strategy of metabolically driven synthetic lethality involving targeting glutamine metabolism for sensitization to venetClax in MM.