Dr. Sohaib A. Khan

Dr. Sohaib A. Khan |Clyto Access

University of Cincinnati College of Medicine, USA

Editorial Board Member

Expertise: Endometrial cancer, Estrogen signaling, Human leukemia, Breast cancer

Dr. Sohaib Khan, Ph.D. is currently Professor and Vice Chair of Cancer and Cell Biology at the University of Cincinnati College of Medicine. Dr. Khan received his Ph.D. degree in Biochemistry from Aligarh University, Aligarh, India in 1974. After a year at the Molecular Biology Division of the Tata Institute of Fundamental Research, Bombay, in 1975 Dr. Khan moved to the U.S. and joined the research staff at Roswell Park Memorial Cancer Institute in Buffalo, New York where his research contributed towards developing terminal transferase, a DNA polymerizing enzyme, as a diagnostic marker for human leukemia. In 1979, Dr. Khan received a second postdoctoral training in molecular biology from Case Western Reserve University. He then moved to the University of Cincinnati College of Medicine in 1980 where he continued his second postdoctoral training. They cloned the APRT gene, showed that a common coding region is present in animal and bacterial phosphoribosyltransferases and described SP-1 response elements in the promoter region of the APRT gene. Incidentally, APRT was among the first few housekeeping genes whose promoter was shown to contain SP-1 responsive “GC boxes”. Further studies showed that the mouse genome also possessed a pseudo-APRT gene. In 1987, he was appointed as an Assistant Professor of Cell Biology, at UC College of Medicine and was promoted to full professor in 2000. Dr. Khan is engaged in understanding the molecular mechanisms of estrogen signaling and estrogen receptor action in breast and endometrial cancer. Some of the highlights of his work include (i) demonstration that the expression of c-jun protooncogene is among the first in the cascade of events that lead to estradiol-induced uterine growth demonstration that estrogen receptor forms a ligand-induced homodimer in vivo that is transcriptionally active “F- domain” of ER harbors sequences that play a critical role in receptor dimerization and interaction between the receptor and coactivators. Towards understanding the role of estrogen receptor in breast cancer, his group has recently succeeded in developing an ER-conditional knockout mouse models. These mice lack ER in mature mammary glands and are defective in milk production. This model will facilitate in vivo approaches to understand the role of ER in mammary gland development and breast carcinogenesis.

Related Journals & Conferences :

Current Research and Therapy in Cancer