Associate Professor, Oncology
The Sidney Kimmel Comprehensive Cancer Center
Johns Hopkins University School of Medicine
PIK3CA is a gene that "drives" many cancers. In 2004, Dr. Park’s group was the first to show that it is frequently mutated in human breast cancers. Because it is known to play such an important role in a variety of cancers, drugs that exploit PIK3CA mutations in cancer cells are under development, but so far have failed in clinical trials. As part of his BCRF research, Dr. Park and his team have characterized unique mutations in the PIK3CA gene and how they work to effect breast cancer progression. These studies have led to the discovery that different mutated forms of the gene work with different “partners” in the cell to promote tumor growth. This could be very important in how tumors respond to treatment and could lead to the development of even more specific targeted therapies. In the coming year, they will continue their work in this area by 1) testing new drugs to target molecules that work with mutant PI3KC to improve the effectiveness of anti-PI3KC therapies and 2) testing new technology that can detect PIK3CA mutations in the blood of patients with metastatic breast cancer (so-called liquid biopsy), replacing the need for tissue biopsy for PIK3CA mutation detection.
Dr. Park is from Saginaw, MI and received his Bachelor’s degree from The University of Chicago in 1989. He then completed a dual MD-PhD training program at The University of Pennsylvania School of Medicine, graduating in 1995. After completing a residency in Internal Medicine and Hematology/Oncology Fellowship Training at The Hospital of The University of Pennsylvania, he finished a postdoctoral research fellowship in cancer genetics in the laboratory of Dr. Bert Vogelstein at Johns Hopkins University. In 2002, Dr. Park joined the faculty in the Department of Oncology at The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins within the Breast Cancer Research Program. His laboratory research focuses on finding mutated or altered genes that are responsible for breast cancer initiation and progression, as well as genes that are mutated leading to chemo- and hormonal drug resistance.