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Scott Powers

Research Professor
Ph.D., Columbia University, 1983


Contact
powers@cshl.edu
(516) 422-4085 (p)
 
My lab is applying genome-wide “big-picture” methods to the study of cancer.  This means we investigate both genetic alternations that promote cancer, as well as factors in the tumor environment that affect cancer proliferation and tumor response to anticancer therapeutics. We have performed integrative functional studies that have revealed oncogenic mechanisms in breast, liver, colon and lung cancers.
Scott Powers’ work focuses on gene alterations that cause cancer and factors that influence responses to specific anticancer drugs. His lab uses technologies that probe the entire genome to identify candidate cancer genes and evaluate their functional role in cell transformation and tumor biology. They also use whole-genome technologies to guide development of novel cancer diagnostics and therapeutics. Using DNA copy number analysis, the Powers group pinpoints novel amplified oncogenes and then applies functional studies to address the mechanisms by which they are implicated in oncogenesis. They have successfully applied this approach in breast, liver, colon, and lung cancers. Powers has also had an important role in the development of a distinctive CSHL approach to functional study of cancer genes. Called integrative oncogenomics, it is a rapid, large-scale screen for genes that are deleted or amplified in human cancers and suspected of being tumor suppressors, in the case of deletions, or oncogenes, in the case of amplifications.

Li, J., Yang, Y., Peng, Y., Austin, R. J., van Eyndhoven, W. G., Nguyen, K. C., Gabriele, T., McCurrach, M. E., Marks, J. R., Hoey, T., Lowe, S. W. and Powers, S. 2002. Oncogenic properties of PPM1D located within a breast cancer amplification epicenter at 17q23. Nat Genet 31: 133-134.

van der Horst, E. H., Degenhardt, Y. Y., Strelow, A., Slavin, A., Chinn, L., Orf, J., Rong, M., Li, S., See, L. H., Nguyen, K. Q., Hoey, T., Wesche, H. and Powers, S. 2005. Metastatic properties and genomic amplification of the tyrosine kinase gene ACK1. Proc Natl Acad Sci U S A 102: 15901-15906.

Kendall, J., Liu, Q., Bakleh, A., Krasnitz, A., Nguyen, K. C., Lakshmi, B., Gerald, W. L., Powers, S. and Mu, D. 2007. Oncogenic cooperation and coamplification of developmental transcription factor genes in lung cancer. Proc Natl Acad Sci U S A 104: 16663-16668.

Zender, L., Xue, W., Zuber, J., Semighini, C. P., Krasnitz, A., Ma, B., Zender, P., Kubicka, S., Luk, J. M., Schirmacher, P., McCombie, W. R., Wigler, M., Hicks, J., Hannon, G. J., Powers, S. and Lowe, S. W. 2008. An oncogenomics-based in vivo RNAi screen identifies tumor suppressors in liver cancer. Cell 135: 852-864.

Sawey, E. T., Chanrion, M., Cai, C., Wu, G., Zhang, J., Zender, L., Zhao, A., Busuttil, R. W., Yee, H., Stein, L., French, D. M., Finn, R. S., Lowe, S. W. and Powers, S. 2011. Identification of a therapeutic strategy targeting amplified FGF19 in liver cancer by oncogenomic screening. Cancer Cell 19: 347-358.

Archived Publications