Cathy Mendelsohn, PhD


mendelsohn

Dr. Mendelsohn is a Professor of Urological Sciences in the Departments of Urology, Genetics & Development, and Pathology & Cell Biology

The research in the Mendelsohn lab focused on development of the urinary tract, and identification of progenitors important for urothelial development and homeostasis and cells of origin that contribute to distinct bladder cancer lesions. Her work investigating the cause of obstruction and vesicoureteral reflux using mouse models has led to a deeper understanding of the etiology of theses malformations, which can cause severe kidney disease (Batourina E, et al., Nature Genetics, 2005; Batourina E, et al., Nature Genetics, 2002). Dr. Mendelsohn’s project with the Columbia University O’Brien Center is focused on identification of events and molecular pathways that when abnormal, cause obstruction, including VUR and posterior urethral valves, a rare but serious congenital malformation. She will use mouse models to identify genetic pathways that underlie these abnormalities, which in turn will be used to evaluate mutations in human families with affected individuals, in collaboration with Dr. Gharavi’s group and the Sanna-Cherci group.

Dr. Mendelsohn’s lab has identified adult and embryonic progenitors that generate urothelial cells in the bladder during urinary tract infection and development, respectively (Gandhi et al., Developmental Cell, 2013). An interesting observation from these studies is that retinoids, vitamin A derivatives, are required in progenitor cells in adults, for entry into mitosis. Analysis of gene expression reveals that genes that mediate iron metabolism are dramatically down regulated in mutants with defective retinoid signaling. Dr. Mendelsohn will collaborate with Dr. Barasch looking at the role of iron in regeneration of the urothelium, which may be regulated by retinoid signaling.

The Mendelsohn lab is also interested in identification of progenitors and their associated mutations that drive muscle invasive bladder cancer. Using a mouse model of carcinogenesis together with lineage analysis we find that distinct sub-populations of urothelial cells contribute to distinct types of lesions (Van Batavia et al., Nature Cell Biology, 2014).  We are now analyzing lesions produced in our mouse model to evaluate their similarity or differences with respect to human bladder cancer lesions with the goal of obtaining drivers that promote invasion and metastases.