Shehla Pervin

Shehla Pervin, PhD

Assistant Professor in Residence, Department of Obstetrics and Gynecology
Assistant Professor, Charles Drew University of Medicine and Science



Scientific Interests

Dr. Shehla Pervin's main focus of research is to identify key cell types involved in promoting initiation of human breast tumors and to understand the molecular mechanisms involved during the process. Her research utilizes primary cells obtained from both triple negative and estrogen receptor positive human breast tumors to generate xenografts in nude mice. Her research group seeks to understand the role of key signaling pathways in mammary cancer stem cells and other stromal cells that contribute to tumor initiation and progression. The other interest of her laboratory is to understand mechanisms and cell types that are sensitive to estrogen and promote estrogen-induced human breast tumors. These studies are geared to identify novel targets that could be targeted for early detection and treatment of breast tumors.

Highlighted Publications

Pervin S, Tran A, Tran L, Urman R, Braga M, Chaudhuri G, Singh R. Reduced association of anti-apoptotic protein Mcl-1 with E3 ligase Mule increases the stability of Mcl-1 in breast cancer cells. Br J Cancer. 2011 Jul 26;105(3):428-37. doi: 10.1038/bjc.2011.242. Epub 2011 Jul 5.

Pervin S, Chaudhuri G, Singh R. NO to breast: when, why and why not? Curr Pharm Des. 2010;16(4):451-62.

Pervin S, Tran AH, Zekavati S, Fukuto JM, Singh R, Chaudhuri G. Increased susceptibility of breast cancer cells to stress mediated inhibition of protein synthesis. Cancer Res. 2008 Jun 15;68(12):4862-74.

Pervin S, Singh R, Hernandez E, Wu G, Chaudhuri G. Nitric oxide in physiologic concentrations targets the translational machinery to increase the proliferation of human breast cancer cells: involvement of mammalian target of rapamycin/eIF4E pathway. Cancer Res. 2007 Jan 1;67(1):289-99.

Pervin S, Singh R, Freije WA, Chaudhuri G. MKP-1-induced dephosphorylation of extracellular signal-regulated kinase is essential for triggering nitric oxide-induced apoptosis in human breast cancer cell lines: implications in breast cancer. Cancer Res. 2003 Dec 15;63(24):8853-60.