Max Costa, PhD

Dr. Costa received his Ph.D. in Pharmacology and Biochemistry from the University of Arizona Medical School, Tuscon, AZ, in 1976.

Postdoctoral Training
Dr. Costa was a Postdoctoral Fellow at the University of Arizona Medical School in Tuscon, AZ, 1976-77.

Professor and Chairman
Department of Environmental Medicine
New York University School of Medicine

Director
Nelson Institute of Environmental Medicine
New York University School of Medicine

Deputy Director
NYU Cancer Institute

Professor of Pharmacology
Department of Pharmacology
New York University School of Medicine

Positions and Employment

1. Young Environmental Scientist Award from NIEHS;
2. Kenneth Morgareidge Award from the International Life Sciences Institute;
3. FASEB awarded Burroughs Wellcome Visiting Professor in the Basic Sciences and Distinguished Scientist Speaker;
4. NIH Toxicology Study Section 1991-1995;
5. Ad hoc NIH Chemical Pathology Study Section 1997;
6. ALT Toxicology I Study Section 1997;
7. US EPA Scientific Peer Review Panel 1984-1992;
8. University of California Tobacco-Related Disease Study Section 1991-1997;
9. Member of the Board of Associate Editors for the NIEHS Environmental Health Perspectives;
10. Organized the First, Second and Third International Meeting on Molecular Mechanisms of Metal Toxicity;
11. National Center for Complementary and Alternative Medicine Special Emphasis Panel 2003.

• Costa, M., Gerner, E.W., and Russell, D.H. Cell cycle specific activity of Type I and Type II cyclic adenosine 3’,5’-monophosphate-dependent protein kinases in Chinese hamster ovary cells. J. Biol. Chem. 251:3313-3319 (1976).
  
• Costa, M. and Mollenhauer, H.H. Carcinogenic activity of particulate metal compounds is proportional to their cellular uptake. Science 209:515-517 (1980).
  
• Costa, M. Molecular mechanisms of nickel carcinogenesis. Ann. Rev. Pharmacol. Toxicol. 31:321-337 (1991).
  
• Klein, C.B., Conway, K., Wang, X.W., Bhamra, R.K., Lin, X., Cohen, M.D., Annab, L., Barrett, J.C., and Costa, M. Senescence of nickel-transformed cells by a mammalian X chromosome: Possible epigenetic control. Science 251:796-799 (1991).
  
• Klein, C.B., Frenkel, K., and Costa, M. The role of oxidative processes in metal carcinogenesis. Chem. Res. Toxicol. 4:592-604 (1991).
  
• Salnikow, K., Cosentino, S., Klein, C.B, and Costa, M. The loss of thrombospondin transcriptional activity in nickel-transformed cells. Mol. Cell. Biol. 14:851-858 (1994).
  
• Lee, Y-W., Klein, C.B., Kargacin, B., Salnikow, K., Kitahara, J., Dowjat, K., Zhitkovich, A., Christie, N.T., and Costa, M. Carcinogenic nickel silences gene expression by chromatin condensation and DNA methylation: A new model for epigenetic carcinogens. Mol. Cell. Biol. 15:2547-2557 (1995).
  
• Zhitkovich, A., Voitkun, V., and Costa, M. Formation of the amino acid-DNA complexes by hexavalent and trivalent chromium in vitro: Importance of trivalent chromium and the phosphate group. Biochemistry 35(22):7275-7282 (1996).
  
• Zhou, D., Salnikow, K., and Costa, M. Cap43, a novel gene specifically induced by Ni2+ compounds. Cancer Res. 58:2182-2189 (1998).
  
• Lee, Y-W., Broday, L., and Costa, M. Effects of nickel on DNA methyltransferase activity and genomic DNA methylation levels. Mutat. Res. 415:213-218 (1998).
  
• Broday, L., Lee, Y-W., and Costa, M. 5-azacytidine induces transgene silencing by DNA methylation in Chinese hamster cells. Mol. Cell. Biol. 19(4):3198-3204 (1999).
  
• Salnikow, K., Blagosklonny, M., Ryan, H., Johnson, R. and Costa, M. Carcinogenic nickel induces genes involved with hypoxic stress. Cancer Res. 60:38-41 (2000).
  
• Broday, L., Peng, W., Kuo, M-H., Salnikow, K., Zoroddu, M., and Costa, M. Nickel compounds are novel inhibitors of histone H4 acetylation. Cancer Res. 60:238-241 (2000)..
  
• Salnikow, K., Su, W., Blagosklonny, M., and Costa, M. Carcinogenic metals induce hypoxia-inducible factor-stimulated transcription by reactive oxygen species-independent mechanism. Cancer Res. 60:3375-3378 (2000).
  
• Salnikow, K., Costa, M., Figg, W.D., and Blagosklonny, M.V. Hyperinducibility of hypoxia-responsive genes without p53/p21-dependent checkpoint in aggressive prostate cancer. Cancer Res. 60:5630-5634 (2000).
  
• Cangul, H., Salnikow, K., Yee, H., Zagzag, D., Commes, T., and Costa, M. Enhanced overexpression of a HIF-1ahypoxia-related protein in cancer cells. Environ. Health Perspect. 110(5):783-788 (2002)
  
• Huang, C., Li, J., Ke, Q., Leonard, S.S., Jiang, B-H., Zhong, X-S., Costa, M., Castranova, V., and Shi, X. Ultraviolet-induced phosphorylation of p70^S6K at Thr³⁸⁹ and Thr⁴²¹/Ser⁴²⁴ involves hydrogen peroxide and mammalian target of rapamycin but not Akt and atypical protein kinase C. Cancer Res. 62:5689-5697 (2002).
  
• Salnikow, K., Davidson, T., and Costa, M. The role of hypoxia-inducible signaling pathway in nickel carcinogenesis. Environ. Health Perspect. 110(5):831-834 (2002).
  
• Salnikow, K., Kluz, T., Costa, M., Piquemal, D., Demidenko, Z.N., Xie, K., and Blagosklonny, M.V. The regulation of hypoxic genes by calcium involves c-Jun/AP-1 which cooperates with HIF-1 in response to hypoxia. Mol. Cell. Biol. 22(6):1734-174 (2002).
  
• Feng, Z., Hu., W., Rom, W.N., Costa, M., and Tang, M-s. Chromium(VI) exposure enhances polycyclic aromatic hydrocarbon-DNA binding at the p53 gene in human lung calls. Carcinogenesis 24:771-778 (2003
  
• Salnikow, K., Davidson, T., Zhang, Q., Chen, L.C., Su, W., and Costa, M. The involvement of hypoxia-inducible transcription factor-1-dependent pathway in nickel carcinogenesis. Cancer Res. 63:3524-3530 (2003).
  
• Yan, Y., Kluz, T., Zhang, P., Chen, H., and Costa, M. Analysis of specific lysine histone H3 and H4 acetylation and methylation status in clones of cells with a gene silenced by nickel exposure. Toxicol. Appl. Pharmacol. 190:272-277 (2003).
  
• Zhang, Q., Salnikow, K., Kluz, T., Chen, L.C., Su, W-C., and Costa, M. Inhibition and reversal of nickel-induced transformation by the histone deacetylase inhibitor trichostatin A. Toxicol. Appl. Pharmacol. 192:201-211 (2003).
  
• Davidson, T., Salnikow, K., and Costa, M. Hypoxia inducible factor-1 independent suppression of aryl hydrocarbon receptor-regulated genes by nickel. Mol. Pharmacol. 64:1485-1493 (2003).
  
• Li, J., Chen, H., Tang, M-s., Shi, X., Amin, S., Desai, D., Costa, M., and Huang, C. PI-3K and Akt are mediators of AP-1 induction by 5-MCDE in mouse epidermal Cl41 cells. J. Cell Biol. 165(1):77-86 (2004)
  
• Caruso, R.P., Levinson, B., Melamed, J., Wieczorek, R., Taneja, S., Polsky, D., Chang, C., Zeleniuch-Jacquotte, A., Salnikow, K., Yee, H., Costa, M., and Osman, I. Altered N-myc downstream-regulated gene 1 protein expression in African-American compared with Caucasian prostate cancer patients. Clin. Cancer Res. 10:222-227 (2004).
  
• Li, J., Davidson, G., Huang, Y., Jiang, B-H., Shi, X., Costa, M., and Huang, C. Nickel compounds act through phosphatidylinositol-2-kinase/Akt-dependent, p70^S6k-independent pathway to induce hypoxia inducible factor transactivation and Cap43 expression in mouse epidermal Cl41 cells. Cancer Res. 64:94-101 (2004).
  
• Li, J., Chen, H., Ke, Q., Feng, Z., Tang, M-s., Liu, B., Amin, S., Costa, M., and Huang, C. Differential effects of polycyclic aromatic hydrocarbons on transactivation of AP-1 and NF-kB in mouse epidermal Cl41 cells. Mol. Carcinog. 40:104-115 (2004).
  
• Yan, Y., Chen, H., and Costa, M. Chromatin immunoprecipitation assays. In: Epigenetics Protocols, T. Tollefsbol (ed.), Vol. 287, Chap. 2, Humana Press, Totowa, NJ, 2004, pp. 9-19.
  
• Davidson, T.L., Kluz, T., Burns, F.J., Rossman, T.G., Zhang, Q., Uddin, A., Nadas, A., and Costa, M. Exposure to chromium(VI) in the drinking water increases susceptibility to UV-induced skin tumors in hairless mice. Toxicol. Appl. Pharmacol. 196:431-437 (2004).
  
• Chen, H., Davidson, T., Singleton, S., Garrick, M.D., and Costa, M. Nickel decreases cellular iron level and converts cytosolic aconitase to iron-regulatory protein 1 in A549 cells. Toxicol. Appl. Pharmacol. In press.
  
• Zoroddu, M.A., Peana, M., Kowalik-Jankowska, T., Kozlowski, H., and Costa, M. Nickel(II) binding to Cap43 protein fragments. J. Inorg. Biochem. In press.