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Donald P. Bottaro, Ph.D.

Portait Photo of Donald Bottaro
Urologic Oncology Branch
Staff Scientist (Facility Head)
Center for Cancer Research
National Cancer Institute
Building 10 - Hatfield CRC
Room 2-3952
Bethesda, MD 20892-1107
Phone:  
301-402-6499
Fax:  
301-402-0922
E-Mail:  
dbottaro@helix.nih.gov

Biography

Dr. Bottaro received his BA from The University of Chicago and PhD in Cellular and Molecular Biology from Boston University. For his doctoral research he was named Young Investigator of the Year by the American Microcirculatory Society in 1986. He trained as a postdoctoral fellow at Harvard Medical School before joining the NCI's Laboratory of Cellular and Molecular Biology in 1987, where he helped identify keratinocyte growth factor (KGF), hepatocyte growth factor (HGF) and their respective cell surface receptors. In 2003, Dr. Bottaro joined the NCI's Urologic Oncology Branch, where he continues to study growth factor signaling pathways and their subversion in cancer.

Research

Research in Urologic Oncology Branch is aimed at identifying the genetic and biochemical defects that contribute to genitourinary malignancies, and to translating these discoveries into safe and effective treatment strategies. The discovery of germline mutations in the HGF receptor, Met, that predispose affected individuals to papillary renal cell carcinoma (HPRC) type 1, significantly strengthened mounting evidence of the oncogenic potential of this signaling pathway. Normally, HGF stimulates proliferation, motility and morphogenesis in a wide spectrum of cell types, contributing to embryonic development and to tissue repair in adulthood. Abnormal activation of the HGF pathway has been found in many human cancers, including carcinomas of the bladder, breast, colon, liver, lung, kidney and thyroid, sarcomas of bone and muscle, leukemia, lymphoma, glioblastoma and melanoma. In many of these cancers, HGF/Met signaling drives cell invasiveness and tumor metastasis, advancing disease beyond current effective therapies. Understanding the molecular basis of oncogenic signaling and developing strategies for its selective disruption in cancer are our highest priorities.

This page was last updated on 7/11/2014.