M
Mitali Pandey
Researcher at Case Western Reserve University
Publications - 10
Citations - 698
Mitali Pandey is an academic researcher from Case Western Reserve University. The author has contributed to research in topics: Prostate cancer & LNCaP. The author has an hindex of 7, co-authored 9 publications receiving 611 citations. Previous affiliations of Mitali Pandey include University Hospitals of Cleveland.
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Journal ArticleDOI
Promoter Demethylation and Chromatin Remodeling by Green Tea Polyphenols Leads to Re-expression of GSTP1 in Human Prostate Cancer Cells
TL;DR: It is demonstrated that GTP has dual potential to alter DNA methylation and chromatin modeling, the 2 global epigenetic mechanisms of gene regulation and their lack of toxicity makes them excellent candidates for the chemoprevention of prostate cancer.
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Chamomile, a novel and selective COX-2 inhibitor with anti-inflammatory activity.
TL;DR: The data suggest that chamomile works by a mechanism of action similar to that attributed to non-steroidal anti-inflammatory drugs, including sulindac and a specific COX-2 inhibitor, NS398, that act similarly in LPS-activated RAW 264.7 cells.
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Plant flavone apigenin inhibits HDAC and remodels chromatin to induce growth arrest and apoptosis in human prostate cancer cells: In vitro and in vivo study
TL;DR: It is confirmed for the first time that apigenin inhibits class I HDACs, particularly HDAC1 and HDAC3 and its exposure results in reversal of aberrant epigenetic events that promote malignancy.
Journal ArticleDOI
Green tea and prostate cancer: from bench to clinic.
Mitali Pandey,Sanjay Gupta +1 more
TL;DR: This review provides an in-depth overview of various biochemical and signaling pathways affected by green tea in in vivo and in vitro models of prostate cancer.
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Protection against oxidative DNA damage and stress in human prostate by glutathione S-transferase P1.
Rajnee Kanwal,Mitali Pandey,Natarajan Bhaskaran,Gregory T. MacLennan,Pingfu Fu,Lee Ponsky,Sanjay Gupta +6 more
TL;DR: Results suggest that loss of GSTP1 expression in human prostate cells, a process that increases their susceptibility to oxidative stress‐induced DNA damage, may be an important target for primary prevention of prostate cancer.