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Hybridization of genomic representation from primary breast tumor (red) and normal (green) to a genomic micro-array, showing copy changes varying from loss (shades of green), no loss (yellow), to amplification (shades of red).
Hybridization of genomic representation from primary breast tumor (red) and normal (green) to a genomic micro-array, showing copy changes varying from loss (shades of green), no loss (yellow), to amplification (shades of red). |
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Michael Wigler Professor Ph.D., Columbia University, 1978 Genomics; cancer genes; signal transduction; yeast genetics; bioinformatics. email wigler@cshl.edu, phone (516) 367-8377, fax (516) 367-8381
Selected Publications Sebat, J., Lakshmi, B., Malhotra, D., Troge, J., Lese-Martin, C., Walsh, T., Yamrom, B., Yoon, S., Krasnitz, A., Kendall, J., Leotta, A., Pai, D., Zhang, R., Lee, Y-H., Hicks, J., Spence, S.J., Lee, A.T., Puura, K., Lehtimäki, T., Ledbetter, D., Gregersen, P.K., Bregman, J., Sutcliffe, J.S., Jobanputra, V., Chung, W., Warburton, D., King, M-C., Skuse, D., Geschwind, D.H., Gilliam, T.C., Ye, K., and Wigler, M. 2007. Strong association of de novo copy number mutations with autism. Science 316: 445–449. Pelham, R.J., Rodgers, L., Hall, I., Lucito, R., Nquyen, K.C.Q., Navin, N., Hicks, J., Mu, D., Powers, S., Wigler, M., and Botstein, M. 2006. Identification of alterations in DNA copy number in host stromal cells during tumor progression. Proc. Natl. Acad. Sci. USA 103: 19848–19853. Hicks, J., Krasnitz, A., Lakshmi, B., Navin, N.E., Riggs, M., Leibu, E., Esposito, D., Alexander, J., Troge, J., Grubor,V., Yoon, S., Wigler, M., Ye, K., Børresen-Dale, A-L., Naume, B., Schlicting, E., Norton, L., Hagerstrom, T., Skoog, L., Auer, G., Maner, S., Lundin, P., and Zetterberg, A. 2006. Novel patterns of genomic rearrangement and their association with survival in breast cancer. Genome Res. 16: 1465–1479. Sebat, J., Lakshmi, B., Troge, J., Alexander, J., Young, J., Lundin, P., Maner, S., Massa, S., Walker, M., Chi, M., Navin, N., Lucito, R., Healy, J., Hicks, J., Ye, K., Reiner, A., Gilliam, T.C., Trask, B., Patterson, N., Zetterberg, A., and Wigler, M. 2003. Large-scale copy number polymorphism in the human genome. Science 305: 525–528. 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. |
Our laboratory has for many years studied the molecular basis of cancer,
in particular the genetic mutations that drive the evolution of the cancer
cell. In recent years this has been extended to the study of the genetic
mutations that underlie devastating genetic diseases such as congenital
heart disease and autism. Common to both areas are a set of genome technologies
for measuring copy number variation between cells. With this technique,
the entire genome of the cell can be scanned at very high resolution (Lucito
et al., 2003), and changes in gene copy numbers resulting from deletions
and amplifications can be readily detected. We are applying these methods
to a large set of clinically annotated breast and ovarian cancers, making
correlations with clinical outcome, and discovering new disease causing
genes. The same technique has application in the analysis of spontaneous
mutations in the germ-line. Hence, we are applying the methodology to
finding the lesions causing sporadic genetic disease. The laboratory has
a particularly intense need for bioinformatics and algorithmic interpretation
from genome-wide experimental data.