Tan A. Ince, MD, PhD

Over the past year, Dr. Ince developed a chemically-defined cell culture medium that allowed his team to directly compare genetically identical tumors that were experimentally created from various distinct normal cell types in the human breast. This experiment revealed that tumor cell behavior is strongly influenced by the nature of the normal cell type that serves as the precursor of the tumor cells. Hence, the researchers predict that a comprehensive analysis of various normal cell types in human breast will be important and instructive for understanding the nature of the tumors that arise from these cells. They will continue this research over the coming year and will use BCRF funding to identify the epigenetic changes that are specific to breast tumor stem cells, and examine the contribution of heat shock proteins to breast tumor phenotype.

Bio:
Dr. Ince received a PhD in pharmacology from Cornell University in 1995. For his thesis work he studied drug resistance in cancer, including regulation of multidrug-resistance (MDR) gene, one of the causes of chemotherapy failure in patients. During this work, he identified a novel non-consensus DNA binding sequence for p53 tumor-suppressor gene in the MDR1 gene promoter that may explain one of the reasons of chemotherapy resistance in p53 mutated tumors.

Following post-doctoral fellowship at Memorial Sloan-Kettering Cancer Center and residency in Anatomic Pathology at Massachusetts General Hospital (2000), he completed a subspecialty fellowship in Women's and Perinatal Pathology at Brigham and Women's Hospital, Harvard Medical School, Boston, MA (2001) where he stayed as a staff pathologist.

Dr. Ince received a 5-year KO-8 mentored physician career development award from National Cancer Institute in 2001 and joined the laboratory of Dr. Robert Weinberg at Whitehead Institute as a visiting clinical scientist the same year. Since then, he has been working on new methods that integrate his background in clinical medicine, molecular biology, pharmacology and pathology, in order to develop better models of breast cancer that mimic the behavior of the human disease such as invasion, metastasis and hormone response in model systems.