Adjunct Assistant Professor
Ph.D., New York University, 1993
Genome microarrays; copy number fluctuation; cancer genomics; amplification; deletion; oncogene; tumor suppressor

Genome microarrays; copy number fluctuation; cancer genomics; amplification; deletion; oncogene; tumor suppressor

email This e-mail address is being protected from spambots. You need JavaScript enabled to view it , office (516) 422-4138 lab (516) 422-4115 fax (516) 422-4109

Progression of cancer is a multi-step process where alteration of the genome is the root of the problem. These alterations, whether genetic or epigenetic, accumulate in precancerous cells until the growth of these cells goes unchecked and become cancerous. Identification of these alterations will lead to the discovery of the genes, oncogenes and tumor suppressors responsible for tumor progression.

We have developed several methods to analyze the cancer genome. One method identifies regions that have undergone copy number fluctuation. These regions can be used to identify the genes important to the cancer cell. A second method identifies epigenetic modifications, which although are not changes to the genetic sequence can have far reaching effects on cancer cell. We utilize these methods to gain a complete picture of the cancer genome in the hope of identifying genes involved in carcinogenesis.

We are currently studying ovarian and pancreatic cancer, with two goals in mind. First, we will be analyzing a large set of tumors to identify the genomic regions that are frequently altered to identify gene candidates, which we will then functionally characterize. Second, we plan to identify similarities in genetic fingerprints using informatics methods. This data will be compared to information from clinical collaborators to correlate tumor fingerprints and disease status, ultimately leading to improved diagnostic and treatment strategies.

Please visit Rob's Lab home page.

Selected Publications

Pelham, R.J., Rodgers, L., Hall, I., Lucito, R., Nguyen, K.C.Q., Navin, N., Hicks, J., Mu, D., Powers, S., Wigler, M., and Botstein, D. 2006. Identification of alterations in DNA copy number in host stromal cells during tumor progression. Proc. Natl. Acad. Sci. USA 103: 19848–19853.

Zender, L., Spector, M.S., Xue, W., Flemming, P., Cordon-Cardo, C., Silke, J., Fan, S., Luk, J.M., Wigler, M., Hannon, G.J., Mu, D., Lucito, R., Powers, S., and Lowe, S.W. 2006. Identification and validation of oncogenes in liver cancer using an integrative oncogenomic approach. Cell 125: 1253–1267.

Lakshmi, B., Hall, I.M., Egan, C., Alexander, J., Leotta, A., Healy, J., Zender, L., Spector, M.S., Xue, W., Lowe, S.W., Wigler, M., and Lucito, R. 2006. Mouse genomic representational oligonucleotide microarray analysis: Detection of copy number variations in normal and tumor specimens. Proc. Natl. Acad. Sci. USA 103: 11234–11239.

Olshen, A., Venkatraman, E.S., Lucito, R., and Wigler, M. 2004. Circular binary segmentation for the analysis of array-based DNA copy number data. Biostatistics 4: 557–572.

Lucito, R., Healy, J., Alexander, J., Reiner, A., Esposito, D., Chi, M., Rodgers, L., Brady, A., Sebat, J., Troge, J., West, J., Rostan, S., Nguyen, K.C.Q., Powers, S., Ye, K.Q., Olshen, A., Venkatraman, E., Norton, L., and Wigler, M. 2003. Microarray analysis of genome copy number variation. Genome Res. 13: 2291–2305.