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Ofer Reizes, PhD

Ofer Reizes, PhD

Director, Hybridoma Core 216.445.0880 (o) 216.444.9404 (f)

Professor, Cancer Biology
Member, Molecular Oncology Program

Ofer Reizes, PhD, is a professor-equivalent staff member at the Department of Cellular and Molecular Medicine and the Core Director of Hybridoma at Case Comprehensive Cancer Center. His research focused on the mechanisms underlying obesity, the regulation of body weight, and obesity-associated diseases such as cancer. After his post-doctoral training, he joined the drug discovery division at Procter & Gamble Pharmaceuticals where he expanded his expertise in obesity research. In 2006, Dr. Reizes was recruited by the Cleveland Clinic. Since then, Dr. Reizes has been working on an independent academic research program dealing with the problem of obesity and cancer.

Dr. Reizes earned his BA in molecular and cell biology from the University of Maryland in 1987. He earned his PhD in molecular pharmacology from the University of Texas – Southwestern Medical Center at Dallas in 1993. From 1994 to 1999, he participated in postdoctoral research at the Children’s Hospital Boston and Harvard Medical School. As a postdoctoral fellow, Dr. Reizes identified an unexpected role for the proteoglycan syndecan-3 in central nervous system control of body weight regulation and feeding behavior. This research was later published in the journals Cell and the Journal of Clinical Investigation.

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Dr. Reizes' research focuses on leptin receptors (LepR) and their impact on breast cancer cells. Leptin is a hormone primarily secreted from fat cells and the receptor is a cytokine receptor expressed in brain, periphery, and multiple tumors. Research is now being done on the mechanics of LepR regulation in cancer stem cell self-renewal and tumor progression. The findings indicate that leptin receptor is necessary for maintenance of the master regulating stem cell transcription factors that control self-renewal.

A second focus of the Reizes laboratory is on the intercellular communication gap junction protein connexin 26 and its role in cancer stem cells. The connexin proteins are considered tumor suppressor genes in breast cancer, yet recent findings in the lab challenge this dogma and suggest connexin 26 is procarcinogenic. The studies utilize stem cell reporters developed in the lab designed to track cancer stem cells in real time. This has allowed the lab to identify connexin 26 in cancer stem cells and track it role and mechanisms in these cells. The goal of these studies is to define the key signaling pathways regulated by connexin 26 in promotion of cancer stem cell self-renewal and tumorigenicity.

leptin receptors, LepR, breast cancer, cancer cells, breast cancer cells, leptin, obesity, fat, fat cells, cytokine receptor, LepR regulation, stem cells, connexin 26 intercellular communication gap junction protein, cancer