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Dr. Stephen G. Swisher was born in Brooklyn, New York. He received a Bachelor of Arts and Sciences degree from Stanford University in 1982 and an MD degree from the University of California at San Diego in 1986. He completed a general surgical residency at the University of California at Los Angeles followed by an additional two years in a thoracic oncology postgraduate research program. In 1994, he entered a cardiothoracic residency in Houston, Texas at the Texas Heart Institute and University of Texas MD Anderson Cancer Center with an emphasis on thoracic oncology. After completing his cardiothoracic residency, Dr. Swisher joined the Department of Thoracic and Cardiovascular Surgery at the University of Texas MD Anderson Cancer Center, as an Assistant Professor of Surgery. In 2001 he was promoted to the position of Associate Professor of Surgery and became Director of the Esophageal Cancer Program.
Dr. Swisher is a diplomate of the American Board of Surgery, and is a member of many professional societies including the Phi Beta Kappa Society, the American Medical Association, the Texas Medical Association, the American Association for Cancer Research and the Society of Surgical Oncology.
Information
Stephen G. Swisher, M.D.
Associate Professor and Associate Surgeon
Director, Esophageal Cancer Program
Offices:
Department of Thoracic and Cardiovascular Surgery
The University of Texas M. D. Anderson Cancer Center
1515 Holcombe Boulevard, Box 109
Houston, TX 77030-4095
Phone: (713) 745-4530
Fax: (713) 794-4901
E-mail:sswisher
For appointments please call (713) 792-6161 or (800) 392-1611.
Education:
- Stanford University, Stanford, CA, B.A. 1982
- University of California at San Diego Medical School, San Diego, CA, MD, 1986
Hospital Training:
Internship:
- University of California at Los Angeles Medical Center, 1986-1987, General Surgery
Residencies:
- Fellow, The University of Texas M. D. Anderson Cancer Center, 1994-1996, Thoracic Surgery
- Resident, St. Luke's Episcopal Hospital/Texas Heart Institute, 1994-1996, Thoracic Surgery
- Registrar, Nottingham, United Kingdom, 1991, General Surgery
- Resident, University of California at Los Angeles Medical Center, 1990-1994, General Surgery
- Fellow, University of California at Los Angeles Medical Center, 1988-1990, Surgical Oncology
- Resident, University of California at Los Angeles Medical Center, 1987-88
Board Certifications:
- American Board of Thoracic Surgery, Diplomate, 1997
- American Board of Surgery, Diplomate, 1994
- Texas State Board of Medical Examiners, 1994
- National Board of Medical Examiners, Diplomate, 1987
- California State Board of Medical Examiners, 1987
Clinical Interests:
Research Interests:
Gene therapy, bcl-2 gene, p53 gene
Recent studies in molecular biology have demonstrated a genetic basis for the development of lung cancer in which various genes are altered, leading to a malignant phenotype. Even though multiple genetic defects are usually present, correction of just one genetic defect is often enough to reverse the malignant phenotype and induce apoptosis, or programmed cell death. Recent advances in gene therapy technology have made gene therapy strategies feasible for the clinic as well as the laboratory. Therefore, my research interests focus on developing novel gene therapy strategies that can be translated into clinical trials.
We recently completed a phase I trial in which 52 patients with advanced non-small cell lung cancer in whom all conventional treatments had failed were injected with adenoviral p53 (Adp53) constructs alone or in combination with cisplatin. Toxicity was minimal, and several patients demonstrated significant tumor regression. Because of these encouraging results, we have initiated a new trial evaluating the efficacy of Adp53 in combination with radiotherapy for definitive treatment of patients with non-small cell lung cancer.
The safety of these strategies also leaves open the possibility that other genes besides wild-type p53 may be useful. One potential group of genes that our laboratory has studied is the Bcl-2 family, which contains multiple homologues with either proapoptotic (Bax, Bak, Bik, and Bid) or antiapoptotic (Bcl-2 and Bcl-XL) function. Potential gene therapy strategies include the overexpression of proapoptotic members or the inhibition of antiapoptotic members of the Bcl-2 family. We have recently developed a proapoptotic Bak adenoviral vector that appears capable of inducing apoptosis in both lung cancer and mesothelioma. This novel vector has induced tumor regression in cell lines and subcutaneous mouse tumors. Optimal conditions for minimal toxicity and maximal effect will be determined with the ultimate goal of developing new therapeutic strategies for combating lung cancer.
