F
Fazlul H. Sarkar
Researcher at Wayne State University
Publications - 626
Citations - 48133
Fazlul H. Sarkar is an academic researcher from Wayne State University. The author has contributed to research in topics: Cancer & Pancreatic cancer. The author has an hindex of 114, co-authored 625 publications receiving 44744 citations.
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Journal ArticleDOI
Inhibition of nuclear factor κB activity by genistein is mediated via Notch-1 signaling pathway in pancreatic cancer cells
TL;DR: This article has been retracted at the request of the editor‐in‐chief and author because of a lack of original research.
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Regulation of FOXO3a/β-catenin/GSK-3β signaling by 3,3′-diindolylmethane contributes to inhibition of cell proliferation and induction of apoptosis in prostate cancer cells.
Yiwei Li,Zhiwei Wang,Dejuan Kong,Shalini Murthy,Q. Ping Dou,Shijie Sheng,G. Prem Veer Reddy,Fazlul H. Sarkar +7 more
TL;DR: The results suggest that B-DIM-induced cell growth inhibition and apoptosis induction are partly mediated through the regulation of Akt/FOXO3a/GSK-3β/β-catenin/AR signaling.
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Synthesis, molecular characterization, and biological activity of novel synthetic derivatives of chromen-4-one in human cancer cells.
Vivek Barve,Fakhara Ahmed,Shreelekha Adsule,Sanjeev Banerjee,Sudhir Kulkarni,Prashant Katiyar,Christopher E. Anson,Annie K. Powell,Subhash Padhye,Fazlul H. Sarkar +9 more
TL;DR: In vitro evaluation of copper complexes against hormone-independent and metastatic breast and prostate cancer cells revealed that 7 was the most potent compound which exhibited PKB (Akt protein) inhibitory activities and caused NF-kappaB inactivation in a well-established orthotopic pancreatic tumor model using COLO 357 cells.
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Antitumor and antimetastatic activities of docetaxel are enhanced by genistein through regulation of osteoprotegerin/receptor activator of nuclear factor-κB (RANK)/RANK ligand/MMP-9 signaling in prostate cancer
TL;DR: Genistein could be a promising nontoxic agent to improve the treatment outcome of metastatic prostate cancer with docetaxel and in severe combined immunodeficient (SCID)-human model of experimental prostate cancer bone metastasis.
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Gene expression profiling revealed survivin as a target of 3,3'-diindolylmethane-induced cell growth inhibition and apoptosis in breast cancer cells.
TL;DR: 3,3'-diindolylmethane inhibited cell growth and induced apoptosis in MDA-MB-231 breast cancer cells by down-regulating survivin, Bcl-2, and cdc25A expression and also caused up-regulation of p21(WAF1) expression, which could be responsible for cell cycle arrest.