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.
V Scholar Plus Award- extended funding for exceptional V Scholars
Myeloproliferative neoplasm (MPN) is a chronic blood cancer without curative treatments. In MPN, blood stem cells obtain mutations that result in excessive numbers of blood cells. Mutations in a gene named calreticulin have been recently found in a large percentage of MPN patients. It is unknown how calreticulin mutations drive MPN. Our goal is to identify how calreticulin mutations cause MPN and to develop drugs targeting calreticulin to treat this disease.
V Scholar Plus Award- extended funding for exceptional V Scholars
Kidney cancer is the 8th most common cancer in the USA. Clear cell renal cell carcinoma (ccRCC) is the most common and lethal type of kidney cancer. If ccRCC spreads from the kidney, it becomes incredibly deadly. In addition, the drugs that successfully treat other cancers have no effect on the tumors. The most common gene mutation in ccRCC was discovered over 20 years ago. Figuring out the function of this gene led to the first drugs that successfully treat ccRCC. While this has improved the outcome for ccRCC patients, they still only survive an average of 22 months. Additionally, some patients do not respond to these drugs at all. We need to better understand what makes ccRCC different than other cancers. In addition, we need to understand what makes some ccRCC patients different than other ccRCC patients. Our lab studies a protein called Polybromo-1, which is the second most commonly mutated gene in ccRCC. Our goal is to understand how ccRCC patients with mutations in this gene are unique. From this information, we will figure out how to treat this set of patients using new drugs.
Clinical research is one of the most important ways that we learn what the best treatments are for patients with cancer. Clinical research often tests new types of treatment or new procedures, with the hope that more patients will benefit from the new treatment. Benefits can include improved chances of responding to therapy, fewer side effects and or safer treatments, and most importantly, in some cases, a better chance for cure.
Unfortunately, some groups of patients do not participate in clinical trials. This lack of participation may be due to obstacles or barriers to participation. Barriers can include difficulty in understanding cancer clinical trials or fear of participation in any type of experimental treatment.
The goal of our research project is to develop a better understanding of what barriers may exist in our community (the Greater New Orleans Region) and to develop educational programs to address concerns that some patients may have. We plan to develop a set of educational materials and create opportunities for community education which utilizes both printed materials and live community interactive educational activities.
These actions, if successful, will lead to a greater understanding of cancer clinical trials in cancer and potentially enhance the participation of minority and underrepresented groups in cancer clinical trials.
utilizing Stuart Scott Memorial Cancer Fund matching funds
Lung cancer is more common and deadly in African American patients compared to other racial groups. One reason for this difference may depend on the genetics of the tumor and how genes are expressed. We plan to study lung cancer samples to find differences in genes between African American and Caucasian tumors. We will also use a ‘Just Ask’ cultural training program to improve the engagement of African‐American lung cancer patients in research and tissue banking. Our hope is that this work will improve the understanding of reasons for racial differences in lung cancer. We hope that by studying the gene expression of tumors we will find new ways to treat patients with lung cancer in the future.
The purpose of our study is to test psychosocial interventions to improve quality of life (QOL) (psychological, physical, social and spiritual well-being) for Latinas with breast cancer and their informal caregivers who are helping them during their cancer journey. Latinas and their caregivers often experience severe psychological distress during cancer treatment and this distress can negatively affect health and well-being. Participants in our study are assigned to either an 8-week supportive health education intervention or an 8-week telephone interpersonal counseling intervention. Both the health education and the counseling are provided over the telephone, and each person is called separately. Our trained health care workers call the women and their caregivers at times that are convenient for them. Sessions are about 30 minutes on the phone each week for 8 weeks. Using the telephone to deliver this service removes many of the access barriers normally associated with counseling or health education. In addition to participating in the 8 education or counseling sessions, we will gather biomarkers using saliva at each measurement period to determine if the intervention was effective at the physiological level. We ask the women and their caregivers to complete some questionnaires 4 times over the next 6 months to determine if the intervention was helpful to them. All study related materials, assessments and sessions are conducted in English or Spanish, depending on the person’s preference. At the end of our study, we also tell them about any other clinical trials that may be of interest.
Neuroblastoma is the third most common childhood cancer. Unfortunately, despite intensive treatment, two-thirds of children with advanced neuroblastoma succumb to their disease. New treatment options must be developed to improve outcomes in this devastating disease. This requires a better understanding of how neuroblastoma cells survive in the face of these intensive therapies. N-Myc is a member of a family of proto-oncogenes (genes capable of leading to cancer development) implicated as a cause of several cancers. N-Myc plays a central role in the aggressiveness of neuroblastoma tumors. Children whose neuroblastoma tumors have extra copies of the N-Myc gene (N-Myc amplification) fare worse than children whose tumors have the normal number of N-Myc genes. However, it is unknown why extra N-Myc leads to poor outcomes. Mxi1 is a protein related to the Myc family, however, it counteracts the ability of N-Myc to cause cell growth. Mxi0 is a similar protein, but it does not inhibit N-Myc like Mxi1. In this proposal, we will test the hypothesis that the balance of Mxi1 and Mxi0 expression is important for maintaining normal growth, and that N-Myc alters this balance, leading to treatment resistance. To accomplish this, we developed a new kind of mouse which has its Mxi1 or Mxi0 genes removed. In this project, we will examine the impact of decreasing Mxi1 or Mxi0 expression on neuroblastoma tumor formation and response to treatment, with the overall goal of finding a mechanism to bypass the effects of N-Myc and improve the outcomes of children with neuroblastoma.
V Scholar Plus Award- extended funding for exceptional V Scholars
Aggressive lymphomas are cancers of white blood cells. The most common type is called diffuse large B cell lymphoma (DLBCL). Most patients with DLBCL can be cured by chemotherapy, but some patients either do not respond to treatment or the disease comes back after a certain time (‘relapse’). If we can identify those patients likely to relapse earlier, we hope to improve their chance of survival. Circulating tumor DNA (‘ctDNA’) is DNA that comes from tumor cells and gets in the blood stream. CtDNA in the patient’s blood can be analyzed to get more information about the tumor. In this study, we developed a blood test to profile ctDNA at different stages of the disease and to identify patients at risk for relapse. We found that ctDNA in the patient’s blood contains information that can be used to tell how well the patients will do with chemotherapy. We also observed that analysis of ctDNA over the course of treatment could show how their lymphomas change over time. For example, we detected new mistakes (‘mutations’) in ctDNA that could be used as an early signal to predict that certain treatments would no longer work in these patients. Also, we found that ctDNA in the blood after treatment predicts disease relapse months earlier than any other clinical method. Our test can also give physicians early warning that the tumor is changing from a slow growing to a fast growing lymphoma type. All this information in ctDNA can be used to learn more about lymphoma biology and to find patient groups with high risk for relapse.
V Scholar Plus Award- extended funding for exceptional V Scholars
Gene regulation is vital for our health and abnormal regulations lead to many diseases, including cancer. There are two mechanisms that control genes: Genetic info and epigenetic. Genetic alterations are stable and we cannot target them. However, epigenetic is dynamic as it changes over time. Epigenetic can control gene expression in tissues. It is the loss of this control that causes cancer. In cancer, only select genes are abnormal while the rest are normal. We need to target only abnormal genes. Current therapy is based on chemicals that target all of the genes in the cell. Thus they have side effects. This proposal develops a novel tool that can target a specific gene. Thus, it can correct an aberrant gene only. The tool also has strong therapeutic potential. This will be very valuable for basic research.
Support for the Liposarcoma Genome Project was funded by
Alex Gould and Friends in memory of Kathryn Gould.
Liposarcoma Genome Project – Liposarcoma is the most common type of cancer that arises in soft tissue. These tumors often present as low grade tumors initially, but a subset of patients will experience recurrence of a higher grade tumor. Those patients who recur with higher grade tumors do poorly. Therefore, our research focuses on understanding these high grade tumors. We will explore the genetic changes between the low grade and high grade tumors in order to understand the molecular features that underlie high grade transformation. We will begin by sequencing gene mutations in these tumors and surveying gene activity in each tumor type (Aim 1). Mechanisms that govern which genes are on and off frequently involve how the DNA is packaged and structurally arranged in the cell. Therefore, we will characterize the packaging (chromatin) and structure (topology) of the genomic DNA in these tumors (Aim 2). By elucidating mechanisms by which tumor cells alter gene expression, we will better understand the genes and pathways that sustain them. Finally, we will develop models of these tumors (Aim 3). We can use these models to test driver genes and candidate therapeutic targets identified in our study. We believe that our interdisciplinary team of clinicians and scientists is poised to complete the proposed aims, which should yield important insights into liposarcoma biology and guide future clinical strategies.
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