Ph.D., Tel Aviv University, 1990
email@example.com | (516) 367-6863 (p)
How does cancer arise? It evolves from innocuous beginnings, as healthy cells accumulate mutations and transform into lethal tumor cells. I am developing mathematical and statistical tools to discover key genetic elements involved in the evolution of cancer, and in particular, metastatic tumors.
Alexander Krasnitz and colleagues use mathematical and statistical tools to discover key genetic elements involved in cancer and to understand how cancer cells evolve. Array-based comparative genome hybridization, a technique honed in the Wigler lab, and, more recently, sequencing experiments, have revealed subtle patterns of frequent and widespread aberration in cancer genomes. Krasnitz hypothesizes that recurrent, aberrant genomic loci observed in a range of cancer types are under selection and therefore are enriched in important cancer genes. He has developed a novel, comprehensive methodology to discover such “cores” and has used it to analyze multiple genome data sets in breast, liver, ovarian, and prostate cancer. The results have been shared with cancer biology labs across CSHL, and they have been a key enabling agent of functional studies using mouse models and RNA interference. Krasnitz has begun to apply these novel statistical tools to the latest generation of experimental data, which have characterized tumor samples down to the level of single cells. By interpreting single-cell genomes, he and colleagues seek to learn how specific tumors evolve and how cancer cells migrate to invade adjacent tissues and metastasize.
Navin, N. E. and Kendall, J. T. and Troge, J. E. and Andrews, P. and Rodgers, L. and McIndoo, J. and Cook, K. and Stepansky, A. and Levy, D. and Esposito, D. and Muthuswamy, L. and Krasnitz, A. and McCombie, W. R. and Hicks, J. B. and Wigler, M. H. (2011) Tumour evolution inferred by single-cell sequencing. Nature, 472(7341) pp. 90-94.
Navin, N. E. and Krasnitz, A. and Rodgers, L. and Cook, K. and Meth, J. L. and Kendall, J. T. and Riggs, M. and Eberling, Y. and Troge, J. E. and Grubor, V. and Levy, D. and Lundin, P. and Månér, S. and Zetterberg, A. and Hicks, J. B. and Wigler, M. H. (2010) Inferring tumor progression from genomic heterogeneity. Genome Research, 20(1) pp. 68-80.
Zender, L. and Xue, W. and Zuber, J. and Semighini, C. P. and Krasnitz, A. and Ma, B. and Zender, P. and Kubicka, S. and Luk, J. M. and Schirmacher, P. and McCombie, W. R. and Wigler, M. H. and Hicks, J. B. and Hannon, G. J. and Powers, S. and Lowe, S. W. (2008) An Oncogenomics-Based In Vivo RNAi Screen Identifies Tumor Suppressors in Liver Cancer. Cell, 135(5) pp. 852-864.
Xue, W. and Krasnitz, A. and Lucito, R. and Sordella, R. and Van Aelst, L. and Cordon-Cardo, C. and Singer, S. and Kuehnel, F. and Wigler, M. H. and Powers, S. and Zender, L. and Lowe, S. W. (2008) DLC1 is a chromosome 8p tumor suppressor whose loss promotes hepatocellular carcinoma. Genes and Development, 22(11) pp. 1439-44.
Hicks, J. B. and Krasnitz, A. and Lakshmi, B. and Navin, N. E. and Riggs, M. and Leibu, E. and Esposito, D. and Alexander, J. and Troge, J. E. and Grubor, V. and Yoon, S. and Wigler, M. H. and Ye, K. and Borresen-Dale, A. L. and Naume, B. and Schlicting, E. and Norton, L. and Hagerstrom, T. and Skoog, L. and Auer, G. and Månér, S. and Lundin, P. and Zetterberg, A. (2006) Novel patterns of genome rearrangement and their association with survival in breast cancer. Genome Research, 16(12) pp. 1465-79.Additional materials of the author at
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