BELINSKY, STEVEN A., PHD

EDUCATION
B.S. (Zoology) 1978, The University of North Carolina
Ph.D. (Toxicology) 1984, The University of North Carolina


 

EMPLOYMENT

 

2014 - present President, Lovelace Biomedical and Environmental Research Institute
2013 - present Co-Director, Cancer Genetics, Epigenetics, and Genomics Research Program for the University of New Mexico Cancer Center
2011 - 2014 Vice President Lovelace Biomedical and Environmental Research Institute
2010 - present Vice President for Academic Research, Lovelace Respiratory Research Institute
2007 - 2013 Associate Director, Johns Hopkins Lung SPORE
2002 - 2013 Co-Director, Population Sciences Program for the University of New Mexico Cancer Center, Albuquerque, NM
2001 - 2007 Deputy Director, New Mexico National Institute Environmental Health Sciences Center, Albuquerque, New Mexico
1998 - Present Senior Scientist, Lovelace Respiratory Research Institute, Albuquerque, New Mexico
1997 - Present Director, Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico
1990 - 1998 Scientist, Lovelace Respiratory Research Institute, Albuquerque, New Mexico
1986 - 1990 Senior Staff Fellow, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina.    
1984 - 1986 Postdoctoral Fellow, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina.
1980 - 1984 Graduate Student, Curriculum in Toxicology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
1978 - 1979 Research Technician, Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.

 

PROFESSIONAL AFFILIATIONS
American Association for Cancer Research
International Association for the Study of Lung Cancer
East Coast Oncology Group
Environmental Mutagen Society
American Society for Clinical Oncologists

AREAS OF RESEARCH

Dr. Belinsky received his undergraduate training and graduate degrees at the University of North Carolina at Chapel Hill.  He then did a postdoctoral fellowship and was a Senior Staff fellow at the National Institute of Environmental Health Sciences before moving to the Lovelace Respiratory Research Institute in Albuquerque, NM in 1990.  He is currently Vice President for Research, Director of the Lung Cancer Program, and co-directs the Cancer Genetics and Epigenetics Program for the University of New Mexico Cancer Center.  He has served on numerous advisory boards for the National Institute of Environmental Health Sciences and the National Cancer Institute.  Dr. Belinsky has worked in the field of tobacco carcinogenesis for >25 years and is internationally recognized for his work in lung cancer and translational studies for early detection of lung cancer.  His laboratory was the first to demonstrate that the tobacco specific nitrosamine causes DNA adducts that accumulate in the lung and lead to mutation of the K-ras oncogene.  His work has been extended to evaluate epigenetic mechanisms for lung cancer, specifically inactivation of genes through aberrant promoter hypermethylation.  Key findings from his laboratory include, identifying the p16 tumor suppressor gene as an early event in lung, the detection of promoter methylation of specific genes up to 3 years prior to diagnosis of lung cancer, and the demonstration that inhibitors that block promoter hypermethylation can prevent lung cancer development.  Currently, his research is focused on controlling lung cancer through the identification of gene targets and pathways that are disrupted during the development of this disease.  These findings are translated into population-based studies for the purpose of developing intermediate biomarkers for predicting cancer risk, early detection, prognosis, and response to preventive interventions.  In addition, his group is involved in conducting at both the animal and human level the evaluation of novel preventive and chemotherapy approaches to reduce the mortality from lung cancer.  Dr. Belinsky has authored more than 200 publications.

Dr. Belinsky also co-directs the Cancer Genetics, Epigenetics, and Genomics (CGEG) Program with Mary Ann Osley at the University of New Mexico.  This is one of the four programs within the NCI designated University of New Mexico Cancer Center. CGEG is a trans-disciplinary program that used genetic, biochemical and genomic approaches to understand cancer susceptibility, etiology, and progression.  Studies are focused on identifying diagnostic and prognostic biomarkers and therapeutic targets with the goal of translating these discoveries to clinical and community interventions.  Work within CGEG examines unique patterns of gene expression in normal and cancer cells, defines pathways that regulate genomic stability and response to environmental carcinogens.

 

ACCESS THIS AUTHOR'S PUBLICATIONS IN PUBMED


REPRESENTATIVE PUBLICATIONS

  1. Belinsky, S.A., Nikula, K.J., Palmisano, W.A., Michels, R., Saccomanno, G., Gabrielson, E., Baylin, S.B., and Herman, J.G.  Aberrant methylation of p16INK4a is an early event in lung cancer and a potential biomarker for early diagnosis.  Proc. Natl. Acad. Sci. (USA) 95: 11891-11896 (1998).
  2. Palmisano, W.A., Divine, K.K., Saccomanno, G., Gilliland, F.D., Baylin, S.B., Herman, J.G., and Belinsky, S.A.  Predicting lung cancer by detecting aberrant promoter methylation in sputum. Cancer Res. 60: 5954-5958, 2000.
  3. Belinsky, S.A., Klinge, D.M., Stidley, C.A., Issa, J-P., Herman, J.G., March, T.H., and Baylin, S.B. Inhibition of DNA methylation and histone deacetylation prevents murine lung cancer. Cancer Res., 63: 7089–7093, 2003.
  4. Belinsky, S. A. Gene promoter hypermethylation as a biomarker in lung cancer.  Nature Rev., 4: 707–717, 2004.
  5. Hutt, J.A., Vuillemenot, B.R., Barr, E.B., Grimers, M., Hahn, F.F., Hobbs, C.H., March, T.H., Gigliotti, A.P., Seilkop, S.K. Finch, G.L, Mauderly, J.L., and Belinsky, S.A.  Life-span inhalation exposure to mainstream smoke induces lung cancer in B6C3F1 mice through genetic and epigenetic pathways.  Carcinogenesis 26: 1999-2009, 2005.
  6. Belinsky, S.A. Silencing of genes by promoter hypermethylation: Key event in rodent and human lung cancer. Carcinogenesis 26: 1481-1487, 2005.
  7. Belinsky, S.A., Klinge, D.M., Dekker, J.D., Smith, M.W., Bocklage, T.J., Gilliland, F.D., Crowell, R.E., Karp, D.D., Stidley, C.A., and Picchi, M.A.  Gene promoter methylation in plasma and sputum increases with lung cancer risk.  Clin. Cancer Res. 11: 6505 - 6511, 2005.
  8. Belinsky, S.A., Liechty, K.C., Gentry, F.D., Wolf, H.J., Rogers, J., Vu, K., Haney, J., Kennedy, T.C., Hirsch, F.R., Miller, Y., Franklin, W.A., Herman, J.G., Baylin, S.B., and Byers, T.  Promoter hypermethylation of multiple genes in sputum precedes lung cancer incidence in a high-risk cohort.  Cancer Res. 66: 3338-3344, 2006.
  9. Belinsky, S.A., Grimes, M.J., Casas, E., Stidley, C.A., Franklin, W.A., Bocklage, T.J., Johnson, D.A., and Schiller, J.H. Predicting gene promoter methylation in lung tumors by evaluating sputum and serum. British J. Cancer. 96: 1278-1283, 2007.
  10. Brock, M.V., Hooker, C.C, Ota, E., Han, Y. Guo, M., Ames, S. Glockner, Piantadosi, S., Gabrielson, E., Belinsky, S.A., Yang, S.C., Baylin, S.B., and Herman, J.G. Using DNA methylation markers to predict early recurrence and to re-stage patients with stage I lung cancer.  New Eng. J. Med. 358: 1118-1128, 2008.
  11. Leng, S., Stidley, C., Willink, R., Bernauer, A., Do, K., Picchi, M., Vandenberg, D., Gilliland, F.D., Crowell, R.E., and Belinsky, S.A. Double-strand break damage and associated DNA repair genes predispose smokers to gene methylation.  Cancer Res. 68:3049-3056, 2008.
  12. Tessema, M., Yu, Y., Stidley, C., Machida, E.O., Schuebel, K.E., Baylin, S.B., and Belinsky, S.A. Concomitant promoter methylation of multiple genes in lung adenocarcinomas from current, former, and never smokers. Carcinogenesis 30: 1132-1138, 2009.
  13. Tessema, M., Klinge, D.M., Yingling, C.M., Do, K., Van Neste, L., and Belinsky, S.A. Re-expression of the CXCL14 chemokine, a common target for epigenetic silencing in lung cancer induces tumor necrosis. Oncogene 29:5159-5170, 2010.
  14. Belinsky, S.A., Grimes, M.J., Picchi, M.A., Mitchell, H.D., Stidley, C.A., Tellez, C.S., Tesfaigzi, Y., Carter, M.M., Casero, R.A., Baylin, S.B., Reed, M.D., and March, T.H. Combination therapy with vidaza and entinostat suppresses tumor growth and reprograms the epigenome in an orthotopic lung cancer model.  Cancer Res. 71:454-462, 2011.
  15. Tellez, C. S., Juri, D.E., Do, K., Bernauer, A., Thomas, C., Damiani, L.A., Tessema, M., Leng, S., and Belinsky, S.A. Carcinogen exposure induces EMT through epigenetic silencing of miR-205 and miR-200 family and promotes stem-like phenotype during transformation of lung epithelial cells. Cancer Res.71:3087-3097, 2011.
  16. Juergens, R.A., Wrangle, J., Vendett, B.S., Murphy, S., Zhao, M., Belinsky, S.A., Herman, J.G., Baylin, S.B., Brock, M.V., and Rudin, C.M.  Combination epigenetic therapy has efficacy in patients with refractory advanced non-small cell lung cancer. Cancer Discovery 1:598-607, 2011.
  17. Leng, S., Do, K., Yingling, C.M., Picchi, M.A., Wolf, H.J., Kennedy, T.C., Feser, W.J., Baron, A.E., Franklin, W.A., Brock, M.V., Herman, J.G., Baylin, S.B., Byers, T., Stidley, C.A., and Belinsky, S.A. Defining a gene promoter methylation signature in sputum for lung cancer risk assessment. Clin. Cancer Res. 18: 3387-3395, 2012.
  18. Leng, S., Stidley, C.A., Willink, R.P., Liu, Y. Picchi, M.A., Edlund, C.K., Van Den Berg, D., Tesfaigzi, Y., Crowell, R.E., Gilliland, F.D., and Belinsky, S.A. Sequence variation in DNA replication and apoptosis genes affects promoter hypermethylation in sputum from lung cancer-free smokers.  Cancer Res., 72: 707-715, 2012.
  19. Reed, M.D., Tellez, C.S., Grimes, M.J., Picchi, M.A., Monseur, H.M., Cheng, Y.S., March, T.H., Kuehl, P.J., and Belinsky, S.A. Aerosolized vidaza suppresses tumor growth and reprograms the epigenome in an orthotopic lung cancer model. Br. J. Cancer 109: 1775-1781, 2013.
  20. Tellez, C.S., Grimes, M.J., Picchi, M.A., Liu, Y., March, T.H., Oganesian, A., Taverna, P., and Belinsky, S.A. SGI-110 and entinostat reduces lung tumor burden and reprograms the epigenome. Int. J. Cancer 135:2223-2231, 2014.