Mutations in a signalling pathway

D. Williams Parsons, Tian-Li Wang, Yardena Samuels, Alberto Bardelli, Jordan M. Cummins, Laura DeLong, Natalie Silliman, Janine Ptak, Steve Szabo, James K. V. Willson, Sanford Markowitz, Kenneth W. Kinzler, Bert Vogelstein, Christoph Lengauer and Victor E. Velculescu
Additional contact information
D. Williams Parsons: The Johns Hopkins University Medical Institutions
Tian-Li Wang: The Johns Hopkins University Medical Institutions
Yardena Samuels: The Johns Hopkins University Medical Institutions
Alberto Bardelli: The Johns Hopkins University Medical Institutions
Jordan M. Cummins: The Johns Hopkins University Medical Institutions
Laura DeLong: The Johns Hopkins University Medical Institutions
Natalie Silliman: The Johns Hopkins University Medical Institutions
Janine Ptak: The Johns Hopkins University Medical Institutions
Steve Szabo: The Johns Hopkins University Medical Institutions
James K. V. Willson: Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center
Sanford Markowitz: Howard Hughes Medical Institute and Ireland Cancer Center, University Hospitals of Cleveland and Case Western University
Kenneth W. Kinzler: The Johns Hopkins University Medical Institutions
Bert Vogelstein: The Johns Hopkins University Medical Institutions
Christoph Lengauer: The Johns Hopkins University Medical Institutions
Victor E. Velculescu: The Johns Hopkins University Medical Institutions

Nature, 2005, vol. 436, issue 7052, 792-792

Abstract: Abstract Protein kinases are enzymes that are important for controlling cellular growth and invasion1, and their malfunction is implicated in the development of some tumours. We analysed human colorectal cancers for genetic mutations in 340 serine/threonine kinases and found mutations in eight genes, including in three members of the phosphatidylinositol-3-OH kinase (PI(3)K) pathway. The discovery of this mutational activation of a key cell-signalling pathway may provide new targets for therapeutic intervention.

Date: 2005
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DOI: 10.1038/436792a

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