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Parmanand Malvi

Researcher at University of Alabama at Birmingham

Publications -  24
Citations -  993

Parmanand Malvi is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Melanoma & Cancer. The author has an hindex of 13, co-authored 21 publications receiving 725 citations. Previous affiliations of Parmanand Malvi include National Center for Charitable Statistics & Yale University.

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Oncogene-directed alterations in cancer cell metabolism.

TL;DR: Evidence for oncogene-directed cancer metabolic regulation is presented and the importance of identifying underlying mechanisms that can be targeted for developing precision cancer therapies is discussed.
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AMPK maintains energy homeostasis and survival in cancer cells via regulating p38/PGC-1α-mediated mitochondrial biogenesis.

TL;DR: Evidence is provided that AMPK-p38-PGC-1α axis, by regulating energy homeostasis, maintains survival in cancer cells under glucose-limiting conditions and signifies the fundamental role of AMPK in controlling cellular bioenergetics and mitochondrial biogenesis incancer cells.
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Heparan Sulfate and Heparan Sulfate Proteoglycans in Cancer Initiation and Progression.

TL;DR: The major cell-aut autonomous and cell-non-autonomous roles of HS and HSPGs in cancer are described and therapeutic opportunities for targeting deregulated HS biosynthesis and H SPGs as a strategy for cancer treatment are discussed.
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Cholesterol depletion by methyl-β-cyclodextrin augments tamoxifen induced cell death by enhancing its uptake in melanoma

TL;DR: Treatment with methyl-β-cyclodextrin (MCD), a cholesterol depleting agent, increases the efficacy of tamoxifen in melanoma cells and may provide a unique therapeutic window for improvement in melan cancer treatment.
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Strategy to enhance efficacy of doxorubicin in solid tumor cells by methyl-β-cyclodextrin: Involvement of p53 and Fas receptor ligand complex

TL;DR: Results suggest that MCD enhances the sensitivity to DOX for which wild type p53 is an important determinant, and p53 inhibition by pharmacological inhibitor pifithrin-α or its specific siRNA attenuated p53 function and down-regulated FasR/FasL thereby preventing cell death.