Key Documents
NIH Biosketch available Online
James Ford
- Associate Professor, Medicine - Oncology
- Associate Professor, Genetics
- Associate Professor (By courtesy), Pediatrics
- Member, Bio-X
- Member, Cancer Center
Contact Information
- Clinical Offices
GI Oncology Clinic 875 Blake Wilbur Dr Clinic B Stanford, CA 94305-5820 Telephone Work (650) 498-6000 Fax (650) 725-9113
- Academic Offices
Personal Information Email jmf@stanford.eduAdministrative Contact Donna Galvez Email drgalvez@stanford.edu Tel Work 721-1503Not for medical emergencies or patient use
Clinical Focus
- Cancer > GI Oncology
- Cancer Genetics
- Gastrointestinal Cancers - Genetics
- Gastrointestinal Cancers - Medical Oncology
- Breast Cancer - Genetics
- Ovarian Cancer - Genetics
- Medical Oncology
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
- Board Certification: Medical Oncology, American Board of Internal Medicine (2005)
- SUMC - Graduate Medical Education (1994) CA
- SUMC - Graduate Medical Education (1991) CA
- Stanford University Medical Center (1990) CA
- Yale University School of Medicine-Graduate (1989) CT
- M.D., Yale Medical School Medicine (1989)
Postdoctoral Advisees
Graduate & Fellowship Program Affiliations
Community & International Work
- The Hong Kong High Risk Breast Cancer Programme and Family Registry More »
Web Site Links
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, 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.
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
- Molecular Genetic and Pathological Studies of Anal Tumors Recruiting
- Novel Serum Markers for Monitoring Response to Anti-Cancer Therapy Recruiting
- PII Combination SBRT with TACE for Unresectable Hepatocellular Carcinoma Recruiting
- Ph II of Capecitabine, Carboplatin & Bevacizumab for Gastroesophageal Junction & Gastric Carcinoma Recruiting
- Phase II Capecitabine, Oxaliplatin & Bevacizumab for Metastatic / Unresectable Neuroendocrine Tumors Recruiting
- Phase II Gemcitabine, Carboplatin & PARP Inhibitor BSI-201 in Neoadjuvant Tx of Triple-Neg Breast CA Recruiting
- Comprehensive Screening for Women at High Genetic Risk for Developing Breast Cancer No longer recruiting
- Molecular Genetic Studies of Childhood Brain Tumors and Blood Samples Completed
- Phase I Dose Escalation of Stereotactic Radiosurgical Boost for Locally Advanced Esophageal Cancer No longer recruiting
- Phase I/II PTK787/ZK 222584 and Gemcitabine in Advanced Pancreatic Cancer No longer recruiting
- Safety Study of Cetuximab in combination with Oxaliplatin, Capecitabine, and Radiation Therapy Followed by Surgery for Locally-advanced Rectal Cancer Completed
- Trilogy Stereotactic Body Radiotherapy for Pancreatic Cancer Completed
Publications
- DNA Repair (Amst). 2009; (7): 795-802
- Cancer Res. 2009; (8): 3589-96
- J Natl Cancer Inst. 2009; (15): 1058-65
- J Clin Oncol. 2008; (29): 4752-8
- Cancer. 2008; (7 Suppl): 1850-6
- Ann Surg. 2007; (6): 873-9
- JAMA. 2006; (12): 1521-3
- EMBO J. 2006; (11): 2605-14
- Cancer Res. 2006; (16): 7910-9
- Mol Cell. 2006; (4): 489-99
- Cancer. 2004; (3): 479-89
- Carcinogenesis. 2003; (5): 843-50
- DNA Repair (Amst). 2003; (7): 819-26
- J Biol Chem. 2003; (47): 46906-10
- DNA Repair (Amst). 2003; (9): 947-54
- Proc Natl Acad Sci U S A. 2002; (20): 12985-90
- Nat Genet. 2002; (1): 180-4
- Mol Cell. 2000; (4): 737-44
- Proc Natl Acad Sci U S A. 1999; (2): 424-8
- J Biol Chem. 1997; (44): 28073-80
- Proc Natl Acad Sci U S A. 1995; (19): 8876-80
- Breast Cancer Res Treat. 2009; (3): 683-6
- Colorectal Dis. 2009;
- Cancer. 2009; (3): 665-72
- Clin Nucl Med. 2009; (5): 312-3
- Breast J. 2008 Mar-Apr; (2): 211-4
- Am J Surg Pathol. 2008; (6): 799-809
- Int J Radiat Oncol Biol Phys. 2008; (3): 678-86
- Fam Cancer. 2008; (2): 179-86
- Fam Cancer. 2008; (2): 125-33
- Pediatr Blood Cancer. 2008; (4): 914-6
- Am J Surg Pathol. 2008; (7): 1029-37
- Breast J. 2007 May-Jun; (3): 281-6
- Cancer Genet Cytogenet. 2007; (2): 89-92
- Genet Med. 2007; (11): 752-60
- JAMA. 2007; (21): 2360-72
- Mol Pharmacol. 2007; (5): 1233-40
- Proc Natl Acad Sci U S A. 2007; (49): 19482-7
- J Natl Compr Canc Netw. 2006; (4): 384-420
- J Natl Compr Canc Netw. 2006; (2): 156-76
- Clin Cancer Res. 2006; (11 Pt 1): 3389-93
- Cancer Epidemiol Biomarkers Prev. 2005; (5): 1082-9
- Mutat Res. 2005; (1-2): 195-202
- Health Expect. 2005; (3): 221-33
- Clin Cancer Res. 2005; (15): 5401-9
- Int J Radiat Oncol Biol Phys. 2005; (2): 320-3
- J Clin Oncol. 2005; (24): 5613-9
- Int J Radiat Oncol Biol Phys. 2004; (4): 1017-21
- Int J Radiat Oncol Biol Phys. 2003; (1): 132-7
- Proc Natl Acad Sci U S A. 2003; (17): 9974-9
- J Mol Med. 2003; (11): 700-7
- Mutat Res. 2003; (2-3): 107-14
- J Gastrointest Surg. 2001 Jan-Feb; (1): 27-35
- Arch Surg. 2001; (1): 65-9
- Dis Colon Rectum. 2001; (1): 52-8
- J Biol Chem. 2001; (28): 25813-22
- Am J Clin Oncol. 2001; (2): 155-9
- Int J Radiat Oncol Biol Phys. 2000; (5): 1483-7
- Mol Cell Biol. 2000; (21): 8018-25
- Mol Carcinog. 2000; (1): 17-24
- Mutat Res. 2000; (4): 285-98
- Mol Cell Biol. 2000; (10): 3705-14
- Ann Surg Oncol. 1999 Jan-Feb; (1): 117-22
- Cancer Res. 1998; (4): 599-603
- J Biol Chem. 1998; (50): 33327-32
- Curr Top Microbiol Immunol. 1997; 47-70
- Cancer Treat Res. 1996; 3-38
- Eur J Cancer. 1996; (6): 991-1001
- Hematol Oncol Clin North Am. 1995; (2): 337-61
- Mol Carcinog. 1994; (2): 105-9
- Cytotechnology. 1993; (1-3): 171-212
- Cancer Lett. 1991; (1): 85-94
- Cancer Res. 1991; (1): 67-72
- Pharmacol Rev. 1990; (3): 155-99
- Cancer Res. 1990; (6): 1748-56
- Mol Pharmacol. 1990; (6): 840-7
- J Clin Oncol. 1989; (9): 1359-64
- Mol Pharmacol. 1989; (1): 105-15