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




2007 - Present Associate Director, Johns Hopkins Lung SPORE
2002 - Present Co-Director, Cancer Epidemiology and Control Program, University of New Mexico Cancer Center, Albuquerque, NM
2001 - 2007 Deputy Director, New Mexico National Institute Environmental Health Sciences (NIEHS) Center, Albuquerque, NM
2001 - Present Clinical Professor, College of Pharmacy, University of New Mexico, Albuquerque, NM
1997 - Present Director, Lung Cancer Program; Senior Scientist, Lovelace Respiratory Research Institute, Albuquerque, NM
1997 - Present Adjunct Associate Professor, Department of Biochemistry and Molecular Genetics, University of New Mexico, Albuquerque, NM
1992 - Present Adjunct Associate Professor, Department of Veterinary Pathobiology, Purdue University, West Lafayette, IN
1991 - 2000 Clinical Associate Professor, College of Pharmacy, University of New Mexico, Albuquerque, NM
1991 - Present Associate Scientist, University of New Mexico Cancer Center, Albuquerque, NM
1990 - 1998 Scientist, Lovelace Respiratory Research Institute (formerly Inhalation Toxicology Research Institute), Albuquerque, NM
1986 - 1990 Senior Staff Fellow, NIEHS, Research Triangle Park, NC
1984 - 1986 Postdoctoral Fellow, NIEHS, Research Triangle Park, NC
1980 - 1984 Graduate Student, Curriculum in Toxicology, The University of North Carolina, Chapel Hill, NC
1978 - 1979 Research Technician, Department of Pharmacology, The University of North Carolina, Chapel Hill, NC


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

The general approach of Dr. Belinsky's research is to use in vivo and in vitro animal and human models to identify and define mechanistically genetic and epigenetic changes involved in cancer development and progression. Emphasis is on conducting translational research that can ultimately lead to novel approaches for chemoprevention and intervention. Current areas of research include: 1) using a rodent model to define mechanisms which underlie aberrant CpG island methylation of tumor suppressor genes, 2) modulating cytosine DNA methyltransferase activity and cancer development, 3) transcriptional regulation of the K-ras and p16 genes, 4) identifying chromosome abnormalities in non- or premalignant bronchial epithelial cells from patients at risk for lung cancer that best predict malignancy, 5) defining the role of CpG island methylation of tumor suppressor genes in the development of human adenocarcinoma of the lung and the influence of environmental exposures on which genes are targeted, 6) developing methylation biomarkers that predict lung cancer, and 7) determining interindividual variation in DNA-repair genes and how this relates to lung cancer susceptibility.




  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.