State: California

Funded by The V Foundation Wine Celebration

Funded by The V Foundation Wine Celebration
In honor of Dick Grace and Jason Ferrick

Funded by The V Foundation Wine Celebration
In honor of Joan Rombaur

Funded by The V Foundation Wine Celebration

Funded by the Gastric Cancer Fund

Dr. James M. Ford, M.D., is an Associate Professor of Medicine, Pediatrics and Genetics at Stanford University School of Medicine. He is the Director of the Stanford Cancer Genetics Clinic and the Stanford Clinical Cancer Genomics Program. A recipient of The V Foundation Translational Research grant in 2002, Ford joined the Scientific Advisory Committee in 2003.

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. 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.

Ford graduated Magna Cum Laude with a B.A. degree from Yale University in 1984 and earned his M.D. degree from Yale in 1989. He has been at Stanford ever since, serving as an intern, resident and fellow before earning his postdoc and becoming Assistant Professor in 1998.

Funded by the 2015 Wine Celebration Fund a Need

More children die from brain tumors than any other type of cancer, and the most common type of brain tumor in children is medulloblastoma. Children with medulloblastoma are treated with surgery, radiation, and chemotherapy, and more than 50% of patients survive into adulthood. However, the treatments used for medulloblastoma lead to many long-term side effects, including growth defects, hormone abnormalities, and impaired intelligence. Like all cancers, medulloblastoma is caused by uncontrolled cell growth. Approximately one-third of medulloblastoma cancers arise when a particular signal that tells brain cells to grow, called Hedgehog, gets stuck in the “on” position. We are interested in uncovering exactly how Hedgehog signals tell medulloblastoma cells to grow. To do so, we are investigating how the Hedgehog pathway is activated, and how Hedgehog activation regulates the expression of other signals to influence cell growth. In particular, we are using existing drugs to understand whether block critical mediators of Hedgehog effects blocks the growth of medulloblastoma. Understanding how Hedgehog signals cause cancer may show us how to turn off these signals, and potentially, lead to new therapies for medulloblastoma.

Funded by the 2015 Wine Celebration Fund a Need, including donations raised by the Dick Vitale Gala and Bristol-Myers Squibb

Recent research revealed that malignant gliomas in children often have common gene mutations in a molecule named H3.3, which is a component of the human genome.  Approximately 30% of pediatric glioblastoma and 70% of diffuse intrinsic pontine glioma (DIPG) cases have the same mutation which causes a change in the H3.3 protein. The human immune system, such as T-lymphocytes (T-cells hereafter), do not normally react to normal proteins, but can recognize and attack cells that have abnormal proteins. Therefore, cancer-specific mutations can be suitable targets for cancer immunotherapy, such as cancer vaccines and adoptive T-cell transfer therapy (i.e., infusion of large number of T-cells). Indeed, immunotherapy using patients’ own T-cells that are engineered to recognize cancer cells have shown remarkable success in other cancers, such as acute lymphocytic leukemia in children. However, it is also important to ensure that those T-cells attack tumor cells but not normal cells. We recently found that the common mutation in H3.3 includes cytotoxic T cells which can kill glioma cells that have the mutation but not cells without the mutation.  We are proposing two lines of translational studies. First, we will isolate genes for the T cell receptor which allows the specific recognition of mutated glioma cells. This will lead to a near future development of adoptive transfer immunotherapy. Concurrently, we will design and conduct a pilot vaccine trial using synthetic peptide for the mutated part of H3.3 in children with H3.3-mutated DIPG or high-grade glioma.

Funded by The V Foundation Wine Celebration Vintner Grant
In honor of Ren Harris

Funded by The V Foundation Wine Celebration