Dr. Jack A. Roth
The University of Texas MD Anderson Cancer Center
Department of Thoracic and Cardiovascular Surgery
- Gene therapy
- Molecular biology of lung cancer
- Targeted cancer therapy
One of the major goals of our laboratory is to develop cancer treatment and prevention strategies targeted to specific genetic abnormalities in the cancer cell. The strategy of inactivation or replacement of cancer-causing genes is analogous to the classic concept of gene therapy for replacement of defective or nonfunctioning genes. The gene families implicated in carcinogenesis include dominant oncogenes and tumor suppressor genes. One of the goals of our research effort is to identify critical genes and their products in the lung carcinogenesis pathway and their mechanism of action. Systemic administration of synthetic nanoscale vectors delivering therapeutics to target specific genetic lesions in orthotopic human lung tumor xenograft models is being investigated. Projects include the development of novel gene-delivery systems and studies of the interaction of gene replacement with chemotherapy, radiation, and other targeted agents.
Dai B, Meng J, Peyton M, Girard L, Bornmann WG, Ji L, Minna JD, Fang B, Roth JA. STAT3 mediates resistance to MEK inhibitor through microRNA miR-17. Cancer Res 71(10):3658-68, 5/2011. e-Pub 3/2011. PMCID: Journal in Process.
Katz RL, He W, Khanna A, Fernandez RL, Zaidi TM, Krebs M, Caraway NP, Zhang HZ, Jiang F, Spitz MR, Blowers DP, Jimenez CA, Mehran RJ, Swisher SG, Roth JA, Morris JS, Etzel CJ, El-Zein R. Genetically abnormal circulating cells in lung cancer patients: An antigen-independent fluorescence in situ hybridization-based case-control study. Clin Cancer Res 16(15):3976-3987, 8/2010. e-Pub 7/2010. PMCID: PMC2949278
Meng J, Peng H, Dai B, Guo W, Wang L, Ji L, Minna JD, Chresta CM, Smith PD, Fang B, Roth JA. High level of AKT activity is associated with resistance to MEK inhibitor AZD6244 (ARRY-142886). Cancer Biol Ther 8(21):2073-80, 2009. PMCID: PMC2835993
Yendamuri S, Vaporciyan AA, Zaidi T, Feng L, Fernandez R, Hofstetter WL, Rice DC, Spitz MF, Swisher SG, Walsh GL, Roth JA, Katz RL. 3p22.1 and 10q22.3 deletions detected by fluorescence in situ hybridization (FISH) a potential new tool for early detection of non small cell lung cancer (NSCLC). J Thoracic Oncol 3:979-984, 2008.
Ji, L., and Roth, J.A. Tumor suppressor FUS1 signaling pathway. J Thorac Oncol 3: 327-330, 2008.
Office: MDA (Unit 1489)
M.D. - Johns Hopkins University School of Medicine - 1971