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Carcinogenesis Advance Access originally published online on May 20, 2008
Carcinogenesis 2008 29(6):1087-1091; doi:10.1093/carcin/bgn096
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Defining the blueprint of the cancer genome

Victor E. Velculescu*

Ludwig Center for Cancer Genetics and Therapeutics, The Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA

* To whom correspondence should be addressed. Tel: +410 955 8878; Fax: +410 955 0548; Email: velculescu{at}jhmi.edu

It is widely accepted that cancer is a disease caused by accumulation of mutations in specific genes. These tumor-specific mutations provide clues to the cellular processes underlying tumorigenesis and have proven useful for diagnostic and therapeutic purposes. To date, however, only a small fraction of genes has been analyzed and the number and type of alterations responsible for the development of common tumor types are unknown. The determination of the human genome sequence coupled with improvements in sequencing and bioinformatic approaches have made it possible to examine the cancer cell genome in a comprehensive and unbiased manner. Systematic sequencing studies have been performed on gene families involved in signal transduction in several tumor types, and have now been extended to include the majority of protein-coding genes in breast and colorectal cancers. These analyses have identified new genes and pathways that had not been linked previously to human cancer. One example has been the discovery of genetic alterations in the PIK3CA gene encoding p110{alpha} phosphatidylinositol 3-kinase and in related pathway genes in >30% of colon and breast cancers. These mutational analyses provide a window into the genetic landscape of human cancer, indicate new targets for personalized diagnostic and therapeutic intervention, and suggest lessons for future large-scale genomic analyses in human tumors.

Abbreviations: EGFR, epidermal growth factor receptor; PI3K, phosphatidylinositol 3-kinase

Received April 7, 2008; revised April 7, 2008; accepted April 7, 2008.


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