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James Ford

Academic Appointments

  • Associate Professor of Medicine (Oncology) and of Genetics and, by courtesy, of Pediatrics

Key Documents

Contact Information

  • Clinical Offices
    GI Oncology Clinic 875 Blake Wilbur Dr Clinic B Stanford, CA 94305
    Tel Work (650) 498-6000 Fax (650) 725-9113
  • Academic Offices
    Alternate Contact
    Donna Galvez Tel Work 721-1503
    Not for medical emergencies or patient use

Professional Overview


Dr. Ford is a medical oncologist and geneticist at Stanford, devoted to studying the genetic basis of breast and GI cancer development, treatment and prevention. Dr. Ford graduated in 1984 Magna Cum Laude (Biology) from Yale University where he later received his M.D. degree from the School of Medicine in 1989. He was a internal medicine resident (1989-91), Clinical Fellow in Medical Oncology (1991-94), Research Fellow of Biological Sciences (1993-97) at Stanford, and joined the faculty in 1998. He is currently Associate Professor of Medicine (Oncology) and Genetics, and Director of the Stanford Cancer Genetics Clinic, at the Stanford University Medical Center.

Dr. Ford’s research goals are to understand the role of genetic changes in cancer genes in the risk and development of common cancers. He studies the role of the p53 and BRCA1 tumor suppressor genes in DNA repair, and uses techniques for high-throughput genomic analyses of cancer to identify molecular signatures for targeted therapies. Recently, his team has identified a novel class of drugs that target DNA repair defective breast cancers, and have opened clinical trials at Stanford and nationally using these “PARP inhibitors” for the treatment of women with “triple-negative” breast cancer.

Dr. Ford’s clinical interests include the diagnosis and treatment of patients with a hereditary pre-disposition to cancer. He runs the Stanford Cancer Genetics Clinic, that sees patients for genetic counseling and testing of hereditary cancer syndromes, and enters patients on clinical research protocols for prevention and early diagnosis of cancer in high-risk individuals.

Clinical Focus

  • Cancer> GI Oncology
  • Cancer Genetics
  • Gastrointestinal Cancers - Genetics
  • Gastrointestinal Cancers - Medical Oncology
  • Breast Cancer - Genetics
  • Ovarian Cancer - Genetics
View All 7clinical focus of James Ford

Administrative Appointments

  • Director, Stanford Clinical Cancer Genetics Program (2000 - present)
  • Director, Oncology Fellowship Training Program (2002 - present)
  • Director, Stanford Clinical Cancer Genomics (2013 - present)

Honors and Awards

  • Member, Western Society for Clinical Investigation (2007)
  • Top Doctor for Cancer, Castle Connolly (2008 -)
  • Council Chair, California Breast Cancer Research Program (2009 - 10)
  • Medical Oncology, Best Doctors in America (2013 -)

Boards, Advisory Committees, Professional Organizations

  • Scientific Advisory Board, V Foundation (2006 - present)
  • Board of Directors, Gastric Cancer Foundation (2008 - present)
  • Member, ASCO Cancer Prevention Committee (2013 - present)

Professional Education

Medical Education: Yale University School of Medicine CT (1989)
M.D.: Yale Medical School, Medicine (1989)
Internship: Stanford University Medical Center CA (1990)
Residency: Stanford University School of Medicine CA (1991)
Fellowship: Stanford University School of Medicine CA (1994)
Board Certification: Medical Oncology, American Board of Internal Medicine (2005)

Community and International Work



Scientific Focus

Current Research and Scholarly Interests

The major investigative focus of this laboratory is to explore the mammalian genetic determinants of the inducible response and cellular sensitivity to DNA damaging cytotoxic agents, focusing particularly on the effects of the p53 and BRCA1 gene products on DNA repair and apoptosis. We have found that loss of p53 and BRCA1 function results in defective nucleotide excision repair (NER) of DNA damage. Therefore, we are focused on identifying the molecular mechanisms that regulate DNA repair by these tumor suppressor genes, and how their deficiency impacts human cancer development. In addition, we are exploring ways to exploit the DNA repair deficiency of p53 and BRCA1 mutant cancer cells and to identify cytotoxic drugs that may specifically target these cancer cells. Current research projects include:

Mechanism of p53-dependent DNA repair:
We initially discovered that loss of activity of the p53 tumor suppressor gene results in defective global NER of UVC-induced DNA photoproducts from genomic DNA, but does not effect the preferential transcription-coupled DNA repair of the transcribed strand of expressed genes. These results suggest that mutations of the p53 gene lead to greater genomic instability due to reduced efficiency in DNA repair. A major current objective is to determine the mechanism for the effect of the p53 gene product on global NER. We have recently identified several p53 inducible genes that are involved in DNA repair, including XPE, XPC and GADD45. In addition, we are exploring how p53 may also effect the base excision repair pathway, and transcription-coupled repair following UVB-induced oxidative DNA damage. A number of approaches are being employed, including use of cell lines and animal models with defined genetic alterations in genes that may be involved in this DNA repair pathway, development of cell lines allowing inducible expression of these p53 regulated genes; cDNA microarrary analysis of p53 and DNA damage inducible gene expression, and novel genomics approaches.

DNA damage inducible response pathways: We have employed novel cDNA microarray analysis methods to explore the gene expression responses to various DNA damaging agents (UV, cisplatin, X-rays, etc.) and other cytotoxic drugs (Taxanes). These studies have identified a number of distinctive damage inducible gene expression patterns, as well as specific gene products whose functions we are currently exploring, including those involved in DNA damage induced apoptosis, proteosomal degradation and DNA repair.

Relationships between p53 function and cancer drug resistance:

The majority of cancer chemotherapeutic agents exert their cytotoxic effects through DNA damage, and p53 may effect cellular sensitivity to these drugs. We have shown that cells mutant for p53 function are resistant to the cytotoxic activity of DNA damaging drugs, but are more sensitive to the microtubule inhibitory drug Taxol, than are the same cells in which wild-type p53 expression is induced. Studies to determine the mechanism for this observation are underway, including analysis of the effect of p53 function on taxane induced apoptotic pathways, mitotic spindle checkpoints and regulation of tubulin dynamics. Additional approaches for the targeted elimination of genetically altered tumor cells are being explored, by searching for agents whose action is enhanced by cell cycle checkpoint defects.

DNA repair deficiencies in inherited genetic syndromes:
Specialized molecular techniques for the quantitative analysis of global NER and transcription-coupled DNA repair are being used to identify and characterize DNA repair deficiencies in human and animal tissues due to inherited genetic traits (e.g. xeroderma pigmentosum, Cockayne’s syndrome, Li-Fraumeni syndrome, HNPCC, Breast/Ovary Cancer etc.). Genotype-phenotype relationships between specific mutations and DNA damage response pathways and clinical outcomes will be established.


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