Biography
Gillian Hirst received her Ph.D. at the University of Edinburgh in the ICRF's (now CRUK) Molecular Oncology Unit, where she focused on the analysis and development of estrogen-regulated biomarkers for use in ovarian and breast cancers treated with anti-estrogenic therapies. As a postdoctoral fellow at CRUK Beatson Laboratories, University of Glasgow, she studied the molecular mechanisms of cisplatin resistance in ovarian cancer, with emphasis on the mismatch repair pathway. Building upon this work she studied the genetic susceptibility to DNA damaging agents in Allan Balmain's group here at UCSF. She has over ten years' experience working as a scientific program manager for multi-consortia projects and oversees biomarker development for the I-SPY2 TRIAL for early high-risk breast cancer, as well as multiple research initiatives within the Breast Care Center and the NIH Molecular Characterization of Screen-detected Lesions Consortium.
Dr. Hirst's areas of research interest span the continuum of disease risk in the analysis and development of biomarkers which will lead to better patient stratification and refined treatment interventions.
Research Overview
Dr Hirst has over 15 years of research experience and managing scientific research programs. Her research interest particularly focuses on the molecular genetics of carcinogenesis, particularly as it relates to breast and ovarian cancer and understanding how we can better utilize biomarkers for risk stratification and treatment refinement. As Scientific Program Manager in the I-SPY2 TRIAL she oversees biomarker development and works with investigators from both academia and pharma to analyze data, tumor and liquid biopsy specimen using expression arrays, next-gen sequencing, multiplex-IHC and phospho-protein arrays.
As an investigator on a U01 which is part of the NIH Molecular Characterization of Screen-Detected Lesions (MCL) consortium, her research is focused on building tissue, pathology and imaging resources to assist in the better molecular definition of DCIS and defining who will recur with aggressive invasive cancer or not. The hope is to be able to stratify patients for either less treatment intervention or more at the earliest stages of disease, and to find potentially common drivers of aggressive disease across multiple disease types, as well as markers of indolent disease by looking at both tumor and stromal microenvironment biology.