biography
Dr. Sarkar is currently a Distinguished Professor in the Departments of Pathology and Oncology at Karmanos Cancer Institute, Wayne State University School of Medicine who started his scientific career in 1978 when he completed his Ph.D. thesis work. Dr. Sarkar’s recent research in the last 10 years has also been focused on understanding the molecular mechanism(s) of Epithelial-to-Mesenchymal Transition (EMT), a phenomenon that is reminiscent of cancer stem cells (CSCs) or cancer stem-like cells (CSLCs) within the tumor microenvironment, which are highly resistant to conventional therapeutics. Since nderstanding the molecular mechanism(s) only is not sufficient, his research also extended to the discovery of strategies by which drug-resistant EMT phenotypic cells (CSCs or CSLCs) could be eliminated by novel agents including “natural agents” (Two patents pending on this topic). Dr. Sarkar also discovered early-on that targeting microRNAs (miRNAs) by such agents could become a newer avenues for the treatment of human malignancies. Moreover, Dr. Sarkar have recently developed a novel synthetic derivative of a “natural agent” curcumin named as CDF (3.4-difluorobenozo-curcumin or in short difluorinated curcumin), which is currently being planned for toxicological testing for clinical developmentDr. Sarkar trained numerous pre-doctoral and post-doctoral students throughout the last 25 years at Wayne State UniversityDr. Sarkar’s activities clearly document his leadership expertise, and he really earned his well-deserved national and international stature in cancer research and drug discovery specifically focusing on conditioning the tumor microenvironment
Area of Interest
cancer biology, cancer drug discovery, experimental therapeutics, medicinal chemistry, molecular mechanism of tumor aggressiveness within the tumor microenvironment, pre-clinical model research and conducting clinical trials.
top publication
1 Ahmad A, Sarkar SH, Aboukameel A, Ali S, Biersack B, Seibt S, Li Y, Bao B, Kong D, Banerjee S, Schobert R, Padhye SB, Sarkar FH. Anticancer action of garcinol in vitro and in vivo is in part mediated through inhibition of STAT-3 signaling. Carcinogenesis 2012. PMCID- in process
2.Ahmad A, Sarkar SH, Bitar B, Ali S, Aboukameel A, Sethi S, Li Y, Bao B, Kong D, anerjee S, Padhye SB, Sarkar FH. Garcinol Regulates EMT and Wnt Signaling Pathways In Vitro and In Vivo, Leading to Anticancer Activity against Breast Cancer Cells. Mol Cancer Ther 2012;11:2193-201. PMCID- in process
3.Ali S, Ahmad A, Aboukameel A, Bao B, Padhye S, Philip PA, Sarkar FH. Increased Ras GTPase activity is regulated by miRNAs that can be attenuated by CDF treatment in pancreatic cancer cells. Cancer Lett 2012;319:173-81. PMC3326199
4.Ali S, Banerjee S, Logna F, Bao B, Philip PA, Korc M, Sarkar FH. Inactivation of Ink4a/Arf leads to deregulated expression of miRNAs in K-Ras transgenic mouse model of pancreatic cancer. J Cell Physiol 2012;227:3373-80. PMC3323695
5.Azmi AS, Sarkar FH. Prostate cancer stem cells: molecular characterization for targeted therapy. Asian J Androl 2012;14:659-60. PMCID- in process
6.Azmi AS, Mohammad RM, Sarkar FH. Can network pharmacology rescue neutraceutical cancer research? Drug Discov Today 2012;17:807-9. PMCID- in process
7.Azmi AS, Aboukameel A, Bao B, Sarkar FH, Philip PA, Kauffman M, Shacham S, Mohammad RM. Selective Inhibitors of Nuclear Export Block Pancreatic Cancer Cell Proliferation and Reduce Tumor Growth in Mice. Gastroenterology 2012. PMCID- in process
8.Bao B, Ahmad A, Kong D, Ali S, Azmi AS, Li Y, Banerjee S, Padhye S, Sarkar FH.Hypoxia induced aggressiveness of prostate cancer cells is linked with deregulated expression of VEGF, IL-6 and miRNAs that are attenuated by CDF. PLoS One 2012;7:e43726. PMC3428287
9.Bao B, Wang Z, Ali S, Ahmad A, Azmi AS, Sarkar SH, Banerjee S, Kong D, Li Y, Thakur S, Sarkar FH. Metformin inhibits cell proliferation, migration and invasion by attenuating CSC function mediated by deregulating miRNAs in pancreatic cancer cells. Cancer Prev Res (Phila) 2012;5:355-64. PMCID- in process
10.Bao B, Ali S, Banerjee S, Wang Z, Logna F, Azmi AS, Kong D, Ahmad A, Li Y, Padhye S, Sarkar FH. Curcumin analogue CDF inhibits pancreatic tumor growth by switching on suppressor microRNAs and attenuating EZH2 expression. Cancer Res 2012;72:335-45. PMCID- in process
11.Bao B, Li Y, Ahmad A, Azmi AS, Bao G, Ali S, Banerjee S, Kong D, Sarkar FH.Targeting CSC-Related miRNAs for Cancer Therapy by Natural Agents. Curr Drug Targets 2012. PMCID- in process
12.Bao B, Ahmad A, Li Y, Azmi AS, Ali S, Banerjee S, Kong D, Sarkar FH. Targeting CSCs within the tumor microenvironment for cancer therapy: a potential role of mesenchymal stem cells. Expert Opin Ther Targets 2012;16:1041-54. PMCID- in process
13.Bao B, Azmi AS, Ali S, Ahmad A, Li Y, Banerjee S, Kong D, Sarkar FH. The biological kinship of hypoxia with CSC and EMT and their relationship with deregulated expression of miRNAs and tumor aggressiveness. Biochim Biophys Acta 2012;1826:272-96. PMCID- in process
14.Kashat M, Azzouz L, Sarkar SH, Kong D, Li Y, Sarkar FH. Inactivation of AR and Notch-1 signaling by miR-34a attenuates prostate cancer aggressiveness. Am J Transl Res 2012;4:432-42. PMC3493023
15.Kong D, Heath E, Chen W, Cher ML, Powell I, Heilbrun L, Li Y, Ali S, Sethi S, Hassan O, Hwang C, Gupta N, Chitale D, Sakr WA, Menon M, Sarkar FH. Loss of let-7 up-regulates EZH2 in prostate cancer consistent with the acquisition of cancer stem cell signatures that are attenuated by BR-DIM. PLoS One 2012;7:e33729. PMC3307758