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James M. Ford, MD, FASCO
Professor of Medicine
Pediatrics and Genetics
Director, Stanford Program for Clinical Cancer Genetics
Stanford University School of Medicine
- Seeking to improve risk assessment in high-risk women and families.
- Studies are ongoing to identify disease-causing gene mutations from a high-risk family cancer registry database.
- This research will improve current gene panel testing by assessing the risks associated with gene mutations in families with a high rate of breast cancer.
The most commonly mutated genes in inherited breast cancer are the BRCA genes (BRCA1 and BRCA2). Numerous other gene mutations or variations have been identified and many have become part of multi-gene risk panels without a clear understanding of the risk they pose in causing breast cancer. Dr. Ford is conducting studies to discern the disease-causing risk of ambiguous gene alterations in families with a high incidence of breast cancer so that gene panel tests can better guide preventive strategies.
Full Research Summary
Currently available gene panel tests for assessing the genetic risk of breast cancer are uninformative for most patients, even for those with strong family histories. Emerging technologies allow inexpensive sequencing of multiple genes, but we do not know whether these tests will improve patient care.
Dr. Ford and his team use high-throughput, multi-gene sequencing technology to identify risk-associated gene variants in many breast cancer-related genes. They recently reported that 10-15 percent of women with personal/family history of breast cancer carry a possible pathogenic gene variant, half in genes other than BRCA1/2, including ATM, CDH1, p53, PALB2, CHEK2, and Lynch syndrome genes.
In the coming year, they will determine if these are disease-causing gene mutations by assessing tumor gene mutations and family inheritance patterns in a population-based registry of breast cancer cases and healthy controls. They will also perform “liquid biopsy” analyses of circulating tumor DNA for early detection of cancer in high-risk individuals.
The results will have strong potential to guide the clinical use of emerging genetic tests to better inform patients about risk and preventive strategies.
Dr. Ford is a medical oncologist and geneticist at Stanford, devoted to studying the genetic basis of breast cancer development, treatment and prevention. He graduated from Yale where he received his MD in 1989. He trained clinically in Medicine and Oncology at Stanford followed by a research fellowship in Biological Sciences, and has been on the faculty at Stanford since 1998, currently as an Associate Professor of Medicine (Oncology), Pediatrics (Medical Genetics) and Genetics, and Director, Stanford Program for Clinical Cancer Genetics and Genomics.
Dr. Ford's goals are to understand the role of genetic changes in cancer genes in the risk and development of common cancers. He discovered that the p53 and BRCA1 tumor suppressor genes regulate DNA repair. He is using techniques for high-throughput genomic analyses of cancer to identify molecular signatures for targeted therapies, and whole-genome next-generation DNA sequencing to identify novel germline cancer susceptibility genes.
Dr. Ford's honors and awards include the Etta S. Chidsey Award in Cancer Research from Yale, NIH K08 Clinical Investigator Award, Second Annual Gerald B. Grindey Memorial Young Investigator Award - AACR, Sidney Kimmel Foundation for Cancer Research Scholar Award, Doris Duke Foundation Clinical Scientist Award in Cancer Etiology and Pathogenesis, Burroughs-Wellcome Fund New Investigator Award in Toxicology, and the V Foundation Translational Research Award. Dr. Ford is an Editor for the journal PLoS Genetics, is on the Scientific Review Committee for the V Foundation for Cancer Research, and former Council President of the California Breast Cancer Research Program.