About

James Ford is a medical oncologist and geneticist at Stanford University, specializing in the genetic basis of breast and gastrointestinal (GI) cancer development, treatment, and prevention. He graduated Magna Cum Laude from Yale University in 1984 with a degree in Biology and earned his M.D. from Yale School of Medicine in 1989. Ford completed his internal medicine residency at Stanford (1989-91), followed by a Clinical Fellowship in Medical Oncology (1991-94), and a Research Fellowship in Biological Sciences at Stanford (1993-97). He joined the Stanford faculty in 1998 and currently holds positions as Professor of Medicine (Oncology) and Genetics, as well as Director of the Stanford Cancer Genetics Clinic and the Cancer Genomics Program. His research focuses on understanding the role of genetic changes in cancer genes, particularly p53 and BRCA1, in DNA repair and cancer susceptibility. Ford's laboratory explores the mammalian genetic determinants of cellular responses to DNA damage, emphasizing the effects of p53 and BRCA1 gene products. His work includes studying the regulatory effects of BRCA1 on DNA repair pathways, developing high-throughput genomic analyses to identify molecular signatures for targeted therapies, and investigating the genetic basis of hereditary cancer syndromes. He has contributed to the discovery of small molecules that enhance DNA repair in BRCA1 mutant cells, with potential for cancer prevention. Ford has also led efforts in translating next-generation sequencing into clinical practice for hereditary cancer risk assessment, identifying additional genetic mutations beyond BRCA1/2 that influence cancer susceptibility. Clinically, he runs the Stanford Cancer Genetics Clinic, providing genetic counseling and testing for hereditary cancer syndromes, and directs the Stanford Cancer Genomics Program, performing tumor profiling to identify genetic targets for personalized therapies. His work has significant implications for targeted cancer treatments, especially in breast and GI cancers, and he is actively involved in clinical trials exploring DNA-damaging drugs and PARP inhibitors for cancers with DNA repair deficiencies.

Research topics

• Medicine
• Biology
• Genetics
• Internal medicine
• Oncology
• Computational biology
• Computer Science
• Pathology
• Immunology
• Cancer research
• Gastroenterology
• World Wide Web
• Bioinformatics

Selected publications

• Uterine serous carcinoma and germline genetic testing: patterns of referral, completion and pathogenic variant detection

  Journal of Medical Genetics · 2026-04-29

  article

  Background Current guidelines recommend consideration of germline genetic testing for patients with uterine serous carcinoma (USC) but real-world data are limited on completion rates of testing and pathogenic variant (PV) identification. This study aimed to evaluate the rate of genetic testing referral and completion in a cohort of patients with USC, determine the prevalence of clinically meaningful PVs found on testing and explore factors associated with genetics referral and testing completion. Methods We retrospectively examined the medical records of all individuals diagnosed with USC between 2019 and 2024 seen at a single academic cancer centre. Outcomes of interest included referral for germline genetic testing, completion of testing and testing results. Results Of 131 individuals included, 5 (3.8%) had prior genetic testing and only 45 (34.4%) were recommended to undergo genetic testing or referred to cancer genetics. Younger individuals and those with a personal history of cancer other than USC or family history of breast or ovarian cancer were more likely to be referred. Nine (26.5%) of 34 individuals who completed germline testing had a PV identified in a cancer-related gene, including BRCA1 , BRCA2 , BRIP1 , CHEK2 , MSH6 , PMS2 and ATM . Only a personal history of cancer other than USC was independently associated with the discovery of a PV on germline genetic testing. In those without a prior personal history of cancer, the PV prevalence was 5.6%. Conclusions Given the high prevalence of PVs in this population, germline genetic testing for all patients diagnosed with USC can provide clinically meaningful benefit but is currently underused in practice.

  PublisherDOI

• A SMUG1 Inhibitor Modulates the Excision of Pyrimidine DNA Damage

  ACS Medicinal Chemistry Letters · 2026-05-19

  article
  PublisherDOI

• Figure S1 from A Four Amino Acid Intracellular Motif of VISTA Blocks Growth Receptor Signaling in Cancer Cells to Induce Tumor Suppression

  2025-09-15

  preprintOpen access

  <p>Figure S1</p>

  PublisherOA PDFDOI

• Polyclonal origins of human premalignant colorectal lesions

  Nature · 2025-11-25 · 7 citations

  articleOpen access
  PublisherOA PDFDOI

• Germline genetic testing referral and completion after diagnosis of endometrial cancer under fifty years of age

  Gynecologic Oncology Reports · 2025-06-01

  articleOpen access
  PublisherDOI

• Figure S4 from A Four Amino Acid Intracellular Motif of VISTA Blocks Growth Receptor Signaling in Cancer Cells to Induce Tumor Suppression

  2025-09-15

  preprintOpen access

  <p>Figure S4</p>

  PublisherOA PDFDOI

• Data from The Gastric Cancer Registry: A Genomic Translational Resource for Multidisciplinary Research in Gastric Cancer

  2025-11-26

  articleOpen access

  <div>AbstractBackground:<p>Gastric cancer is a leading cause of cancer morbidity and mortality. Developing information systems which integrate clinical and genomic data may accelerate discoveries to improve cancer prevention, detection, and treatment. To support translational research in gastric cancer, we developed the Gastric Cancer Registry (GCR), a North American repository of clinical and cancer genomics data.</p>Methods:<p>Participants self-enrolled online. Entry criteria into the GCR included the following: (i) diagnosis of gastric cancer, (ii) history of gastric cancer in a first- or second-degree relative, or (iii) known germline mutation in the gene <i>CDH1</i>. Participants provided demographic and clinical information through a detailed survey. Some participants provided specimens of saliva and tumor samples. Tumor samples underwent exome sequencing, whole-genome sequencing, and transcriptome sequencing.</p>Results:<p>From 2011 to 2021, 567 individuals registered and returned the clinical questionnaire. For this cohort 65% had a personal history of gastric cancer, 36% reported a family history of gastric cancer, and 14% had a germline <i>CDH1</i> mutation. 89 patients with gastric cancer provided tumor samples. For the initial study, 41 tumors were sequenced using next-generation sequencing. The data was analyzed for cancer mutations, copy-number variations, gene expression, microbiome, neoantigens, immune infiltrates, and other features. We developed a searchable, web-based interface (the GCR Genome Explorer) to enable researchers’ access to these datasets.</p>Conclusions:<p>The GCR is a unique, North American gastric cancer registry which integrates clinical and genomic annotation.</p>Impact:<p>Available for researchers through an open access, web-based explorer, the GCR Genome Explorer will accelerate collaborative gastric cancer research across the United States and world.</p></div>

  PublisherDOI

• Polyclonal origins of human premalignant colorectal lesions

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-09-12

  preprintOpen access

  ABSTRACT Cancer is generally thought to be caused by expansion of a single mutant cell 1 . However, analyses of early colorectal cancer lesions suggest that tumors may instead originate from multiple, genetically distinct cell populations 2,3 . Detecting polyclonal tumor initiation is challenging in patients, as it requires profiling early-stage lesions before clonal sweeps obscure diversity. To investigate this, we analyzed normal colorectal mucosa, benign and dysplastic premalignant polyps, and malignant adenocarcinomas (123 samples) from six individuals with familial adenomatous polyposis (FAP). Individuals with FAP have a germline heterozygous APC mutation, predisposing them to colorectal cancer and numerous premalignant polyps by early adulthood 4 . Whole-genome and/or whole-exome sequencing revealed that many premalignant polyps—40% with benign histology and 28% with dysplasia—were composed of multiple genetic lineages that diverged early, consistent with polyclonal origins. This conclusion was reinforced by whole-genome sequencing of single crypts from multiple polyps in additional patients which showed limited sharing of mutations among crypts within the same lesion. In some cases, multiple distinct APC mutations co-existed in different lineages of a single polyp, consistent with polyclonality. These findings reshape our understanding of early neoplastic events, demonstrating that tumor initiation can arise from the convergence of diverse mutant clones. They also suggest that cell-intrinsic growth advantages alone may not fully explain tumor initiation, highlighting the importance of microenvironmental and tissue-level factors in early cancer evolution.

  PublisherOA PDFDOI

• PARP inhibitor and PRMT5 inhibitor synergy is independent of BRCA1/2 and MTAP status in breast cancer cells

  Scientific Reports · 2025-10-21

  articleOpen accessSenior author

  PARP inhibitors have been approved for treating a subset of breast cancer patients harboring BRCA1/2 mutations. However, TNBC patients with wildtype BRCA1/2 have limited targeted therapeutic options. Dysregulation of protein arginine methyltransferase 5 (PRMT5) has been implicated in the progression of various cancers, including breast cancer. This study investigates the effects of two classes of PRMT5 inhibitors, GSK3326595 and TNG908, on breast cancer cell lines with different BRCA1/2 statuses to evaluate their therapeutic potential and synergy with PARP inhibitors. A panel of seven breast cancer cell lines was treated with PRMT5 and PARP inhibitors, followed by cell viability measurements using an MTT assay. Drug interactions were analyzed using the Loewe method on the Combenefit Software. Additionally, RT-qPCR was conducted to measure the expression of known DNA damage response genes. Synergy was observed in all cell lines, with BRCA1/2 wildtype cell lines displaying higher synergy scores than BRCA1/2 mutant lines, while the synergy was independent of MTAP status. Mechanistically, PRMT5 inhibition did not alter the early gene expression of known DNA damage response genes as measured by RT-qPCR. Notably, short-term PRMT5 inhibition was sufficient to sensitize an isogenic pair of ovarian cancer cells to subsequent PARP inhibition. These findings highlight the potential of combining PRMT5 inhibitors with PARP inhibitors in a wide range of cancers beyond BRCA1/2 and MTAP mutants. Further investigation is warranted to elucidate the underlying mechanisms of sensitization and the timing of cellular responses to PRMT5 inhibition.

  PublisherOA PDFDOI

• A triple-punch approach: methionine restriction enhances combination inhibitors in brain metastatic triple-negative breast cancer

  Journal of Clinical Investigation · 2025-06-30 · 1 citations

  letterOpen accessSenior author

  Triple-negative breast cancer (TNBC), the most aggressive subtype of breast cancer, presents a clinical challenge in developing effective treatment options. In this issue of the JCI, Zeng et al. demonstrate a provocative and promising therapeutic strategy for TNBC by leveraging the metabolic vulnerabilities presented by methylthioadenosine phosphorylase (MTAP) deletion to genotoxic stress inducers, such as poly (ADP-ribose) polymerase inhibitors (PARPi). They found that combining MTAP deletion or inhibition with PARPi was highly effective in brain metastatic TNBC where the methionine-limited environment further enhanced this combination. This approach underscores the importance of targeting metabolic vulnerabilities in the development of personalized cancer therapies.

  PublisherDOI

Recent grants

• NIH Grant R01CA083889

  NIH · $653k · 2002

• NIH Grant P50MH030854

  NIH · $1.5M · 1998

• NIH Grant R21NS061674

  NIH · $160k · 2012

• EMPOWER Study: Promoting BC Screening in Women Who Survived Childhood Cancer

  NIH · $6.6M · 2009–2023

• NIH Grant R21CA109190

  NIH · $267k · 2008

Frequent coauthors

• Judy E. Garber

  Dana-Farber Cancer Institute

  177 shared

• Laura J. Esserman

  155 shared

• Allison W. Kurian

  Palo Alto University

  155 shared

• Gordon B. Mills

  OHSU Knight Cancer Institute

  152 shared

• Linda Robinson

  The University of Texas Southwestern Medical Center

  148 shared

• Kevin S. Hughes

  Medical University of South Carolina

  148 shared

• Patricia A. Ganz

  University of California, Los Angeles

  145 shared

• David Euhus

  145 shared

Awards & honors

• Member, Western Society for Clinical Investigation (2007)
• Top Doctor for Cancer, Castle Connolly (2008 -)
• Council Chair, California Breast Cancer Research Program (20…
• Medical Oncology, Best Doctors in America (2013 -)
• Editor-in-Chief, JCO Precision Oncology Journal (2016 - 2020…