Personal Statement
I have worked in the field of tobacco carcinogenesis for more than 30 years conducting basic and translational research on lung cancer and received the 2009 Alton Ochsner Award Relating Smoking and Health in recognition of the advances my group has made in tobacco research. My group first demonstrated that the tobacco specific nitrosamine NNK causes DNA adducts that accumulate in the lung due to reduced repair compared to liver and lead to mutation of the K-ras oncogene.
My research in epigenetics began in the 1990s with initial key studies identifying silencing of the p16 gene as an early event in lung cancer, the detection of promoter methylation of specific genes in sputum up to three years prior to clinical diagnosis, and that the combination of a demethylating agent and inhibitor of histone deacetylase can impact lung cancer growth. I have extended all these research areas over more than three decades studying the basic genetics and epigenetics of lung cancer, conducting population-based studies that have identified double-strand break repair as a key determinant of promoter hypermethylation, and developing animal models for evaluating cancer preventives and therapeutics.
I have also developed a pre-malignancy model using immortalized lung epithelial cells to study mechanisms of transformation induced by tobacco and other lung toxicants such as arsenic. Together, these research activities have provided me with the experience and knowledge to serve as a co-leader with Drs. Osley and Ozbun for the Cell and Molecular Oncology Program of the UNM Comprehensive Cancer Center.
Recent work is reflected in the following publications: (1) Tellez, C., Juri, D.E., Do, K., Picchi, M. Spira, A., and Belinsky, S.A. (2016) Mir-196b is epigenetically silenced during the pre-malignant stage of lung cancer. Cancer Res. 76:4741-4751. PMCID: PMC4987256; (2) Filipczak, P.T., Leng, S., Tellez, C.S., Do, T., Grimes, M.J., Thomas, C.L., Walton-Filipczak, S., Picchi, M.A., and Belinsky, S.A. (2019) TET1 is a p53-suppressed oncogene in lung cancer that prevents cellular aging and a target for enhancing therapy-induced senescence. Cancer Res. 79:1758-1768. PMCID: PMC6467797; and (3) Kuehl, P.J., Tellez, C.S., Grimes, M.J., March, T.H., Tessema, M., Revelli, D.A., Mallis, L.M., Dye, W.W., Sniegowski, T., Badenoch, A., Burke, M., Dubose, D., Vodak, D.T., Picchi, M.A., and Belinsky, S.A. (2020) 5-Azacytidine inhaled dry powder formulation profoundly improves pharmacokinetics and efficacy for lung cancer therapy through genome reprogramming. Br J Cancer 122:1194-1204. PMCID: PMC7156464.