Genomic abnormalities presented by cancer cells are many and varied but patterns in these data provide some insight into factors affecting tumor growth and maintenance. For certain allelic loss data and comparative genomic hybridization data I have been working on statistical methods to uncover significant patterns. Here you may find references and software. This work is supported by a grant from the National Cancer Institute, R01 CA64364.

Methodological Manuscripts and Software

• M.A. Newton , H. Yang, P. Gorman, I. Tomlinson, and R. Roylance (2003). A statistical approach to modeling genomic aberrations in cancer cells (with discussion). In Bayesian Statistics 7 , J.M. Bernardo, M.J. Bayarri, J.O. Berger, A.P. Dawid, D. Hecherman, A.F.M. Smith and M. West (Eds.) Oxford University Press.
• M.A. Newton (2002). Discovering combinations of genomic alterations associated with cancer. Journal of the American Statististical Association 97 931-942.
• M.A. Newton. A statistical method to discover significant combinations of genetic aberrations associated with cancer using comparative genomic hybridization profiles. Technical Report 148, Department of Biostatistics and Medical Informatics, October 2001. (Software included.)
• M.A. Newton , and Y. Lee, 2000. Inferring the location and effect of tumor suppressor genes by instability-selection modeling of allelic-loss data. . Biometrics, 56 , 1088-1097.
• M. A. Newton , T. Yeager, and C.A. Reznikoff (1999). A statistical analysis of cancer genome variation. IMA Volumes in Mathematics and its Applications M. Elizabeth Halloran, Seymour Geisser (eds) 112 , 223-236, Springer-Verlag.
• M.A. Newton , M.N. Gould, C. A. Reznikoff, and J.D. Haag (1998). On the statistical analysis of allelic-loss data. Statistics in Medicine 17 , 1425-1445.
• M.A. Newton , S. Q. Wu, and C. A. Reznikoff, 1994. Assessing the significance of chromosome-loss data: Where are the suppressor genes for bladder cancer? Statistics in Medicine, 13, 839-858.

Applications

• J.G. Teeguarden, M.A. Newton , Y.P. Dragan, H.C. Pitot, 2000. Genome-wide loss of heterozygosity analysis of chemically induced rat hepatocellular carcinomas reveals elevated frequency of allelic imbalances on chromosomes 1, 6, 8, 11, 15, 17, and 20. Molecular Carcinogenesis, 28: 51-61.
• D.F. Jarrard, S. Sarkar, Y. Shi, T.R. Yeager, G. Magrane, H. Kinoshita, N. Nassif, L. Meisner, M.A. Newton , F.M. Waldman, and C.A. Reznikoff (1999). p16/pRb Pathway Alterations Are Required for Bypassing Senescence in Human Prostate Epithelial Cells. Cancer Research. 59(12):2957-64.
• T.R. Yeager, S. DeVries, D.F. Jarrard, C. Kao, S.Y. Nakada, T.D. Moon, R. Bruskewitz, W.M. Stadler, L.F. Meisner, K.W. Gilchrist, M.A. Newton , F.M. Waldman, and C.A. Reznikoff (1998). Overcoming cellular senescence in human cancer pathogenesis. Genes and Development, 12, 163--174.
• C. Reznikoff, C. Belair, E. Savelieva, Y. Zhai, K. Pfeifer, T. Yeager, K. J. Thompson, Sandy DeVries, C. Bindley, M.A. Newton , G. Sekhon, and F. Waldman, 1994. Long term genome stability and minimal genotypic and phenotypic alterations in HPV16 E7, but not E6 immortalized human uroepithelial cells. Genes and Development, 8, 2227-2240.