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Dr. Jack A. Roth was born in LaPorte, Indiana. He received his Bachelor of Arts degree from Cornell University in Ithaca, New York and received his MD degree from the Johns Hopkins University School of Medicine. He was a surgical intern and resident at the Johns Hopkins Hospital. He went on to the UCLA Center for the Health Sciences to complete his Postgraduate Research Fellowship, and completed residencies in General Surgery and Thoracic Surgery at the UCLA School of Medicine. Dr. Roth is certified by the American Board of Surgery and American Board of Thoracic Surgery. After completing his residency, Dr. Roth became head of the Thoracic Oncology Section of the Surgery Branch of the National Cancer Institute. In 1986 Dr. Roth became Professor and Chairman of the Department of Thoracic and Cardiovascular Surgery at the University of Texas MD Anderson Cancer Center. He holds the Bud S. Johnson Clinical Chair and is a Professor of Tumor Biology. He is a member of 29 national and international professional associations including the Society of University Surgeons, the American Association for Thoracic Surgery, and the American Surgical Association. He also serves on 14 editorial boards of major clinical and scientific journals including the Journal of Thoracic and Cardiovascular Surgery, the Journal of Molecular Medicine, Clinical Cancer Research, and Cancer Gene Therapy.
Information
Jack A. Roth, M.D.
Professor and Chairman Department of Thoracic and Cardiovascular Surgery
Bud Johnson Clinical Distinguished Chair
Professor of Molecular and Cellular Oncology
Director, W.M. Keck Cancer Center for Cancer Gene TherapyOffices:
Department of Thoracic and Cardiovascular Surgery
The University of Texas M. D. Anderson Cancer Center
1515 Holcombe Boulevard, Box 445
Houston, TX 77030-4095
Phone: (713) 792-7664
Fax: (713) 794-4901
E-mail:jroth
For appointments please call (713) 792-6161 or (800) 392-1611.
Education:
- Cornell University, Ithaca, NY, B.A. 1967
- Johns Hopkins University School of Medicine, Baltimore, MA, MD, 1971
Hospital Training:
Internship:
- Johns Hopkins Hospital, 1971-72, Surgery
Residencies:
- Chief Resident, UCLA School of Medicine, 1979-80, Division of General Surgery
- Chief Resident, UCLA School of Medicine, 1978-79, Division of Thoracic Surgery
- UCLA School of Medicine, 1977-78, Division of Thoracic Surgery
- UCLA School of Medicine, 1975-77, Division of General Surgery
- Research Fellow, UCLA Center for the Health Sciences, 1973-75, Division of Surgical Oncology
- Johns Hopkins Hospital, 1972-73, Surgery
Board Certifications:
- American Board of Thoracic Surgery, Recertification, 1991
- American Board of Thoracic Surgery, Diplomate, 1983
- American Board of Surgery, Diplomate, 1981
Clinical Interests:
Research Interests:
Tumor suppressor genes, gene therapy, lung neoplasms, esophageal neoplasmsCancer is a genetic disease, and one of the most direct preventive and therapeutic approaches to cancer is correction of the genetic lesions responsible for malignant transformation. This has the advantage of developing cancer cell-selective treatments that may work by novel mechanisms. However, efficient and selective delivery of corrective genes to the cancer cell is an ongoing challenge. Our research has focused on the replacement of defective or nonfunctioning genes in the cancer cell. The gene families implicated in carcinogenesis include dominant oncogenes and tumor suppressor genes. We have endeavored to develop viral vectors that can efficiently deliver wild-type tumor suppressor genes to cancer cells. Regional and systemic administration of viral vectors expressing wild-type p53 prevents growth of tumors with mutant p53 in orthotopic tumor models and mediates regression of established apoptosis in tumors when combined with p53 gene restoration. Viral and nonviral vectors expressing a variety of other tumor suppressor and proapoptotic genes are being developed.
These studies provided a rationale for clinical protocols treating non-small cell lung cancer with intralesional injections of both retroviral and adenoviral vectors expressing wild-type p53. The first report of p53 gene replacement using a retroviral vector showed that the treatment was safe, had minimal side effects, and mediated major regressions of tumors refractory to conventional treatment. A second, larger study with an adenoviral vector showed similar results. Future studies will be directed at combining p53 gene replacement with conventional treatments in earlier-stage patients. If these agents are efficacious, their lack of toxicity may provide a sufficiently high therapeutic index such that they could be used as an adjuvant to surgery to treat patients with cancer in early stages or to prevent the development of second primary cancers in individuals with genetic abnormalities in premalignant lesions. The possibility of specific gene targeting with a high therapeutic index makes this a promising area for investigation.