James Ford

Clinical Focus

• Cancer > GI Oncology
• Cancer Genetics
• Gastrointestinal Cancers - Genetics
• Gastrointestinal Cancers - Medical Oncology
• Breast Cancer - Genetics

Administrative Appointments

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

Honors and Awards

• Top Doctor for Cancer, Castle Connolly (2008)
• Member, Western Society for Clinical Investigation (2007)
• Council Chair, California Breast Cancer Research Program (2009 - 10)

Professional Education

Postdoctoral Advisees

Elizabeth Alli , Kedar Hastak , Amy McMullen , Mehrdad Mobasher , Priti Patel , Mahesh Seetharam , Shaveta Vinayak

Graduate & Fellowship Program Affiliations

• Cancer Biology
• Genetics
• Health Research and Policy
• Medicine

Community & International Work

• The Hong Kong High Risk Breast Cancer Programme and Family Registry 

Web Site Links

• Ford Lab Site

Research 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,...

Clinical Trials

• A Phase II Study of GSK1363089 (Formerly XL880) for Metastatic Gastric Cancer Recruiting
• Clinical & Pathological Studies of Upper Gastrointestinal Carcinoma Recruiting
• Phase II Trial - Breast Cancer Chemoprevention by Lovastatin Recruiting
• Assessment of Health Related Quality of Life in Patients Treated for Rectal Cancer Recruiting
• Genome, Proteome and Tissue Microarray in Childhood Acute Leukemia Recruiting

Publications

• The role of the retinoblastoma/E2F1 tumor suppressor pathway in the lesion recognition step of nucleotide excision repair. Lin PS, McPherson LA, Chen AY, Sage J, Ford JM. DNA Repair (Amst). 2009; 8 (7): 795-802
• Defective repair of oxidative dna damage in triple-negative breast cancer confers sensitivity to inhibition of poly(ADP-ribose) polymerase. Alli E, Sharma VB, Sunderesakumar P, Ford JM. Cancer Res. 2009; 69 (8): 3589-96
• Second primary breast cancer occurrence according to hormone receptor status. Kurian AW, McClure LA, John EM, Horn-Ross PL, Ford JM, Clarke CA. J Natl Cancer Inst. 2009; 101 (15): 1058-65
• Performance of BRCA1/2 mutation prediction models in Asian Americans. Kurian AW, Gong GD, Chun NM, Mills MA, Staton AD, Kingham KE, Crawford BB, Lee R, Chan S, Donlon SS, Ridge Y, Panabaker K, West DW, Whittemore AS, Ford JM. J Clin Oncol. 2008; 26 (29): 4752-8
• Hereditary diffuse gastric cancer: implications of genetic testing for screening and prophylactic surgery. Cisco RM, Ford JM, Norton JA. Cancer. 2008; 113 (7 Suppl): 1850-6