P. Sanseau, M. Bernard, Y. Arlot-Bonnemains and C Prigent Pages 271 - 279 ( 9 )
Genetic instability often leads to tumourogenesis. Genomic alterations such as deletions of a chromosome region containing a tumour suppresser gene or amplification of a region containing an oncogene have been frequently found to be associated with the initiation and the progression of cancer. Therefore identification of chromosomal regions amplified or deleted in tumour cells may reveal the presence of such genes. Amplification of 20q13 for instance is frequently observed in breast cancer cells. This region contains a gene encoding a protein kinase that belongs to the Aurora/Ipl1p-related kinase family involved in microtubule dependent mitotic events that control chromosome segregation. Deregulation of these kinases perturbs the ploidy of the cells. The human genome encodes at least three different kinases that have been found to be overexpressed in different tumour cells. But only the ectopic overexpression of the kinase encoded by the gene located at 20q13 is capable to transform cultured cells an d induce the apparition of tumours in nude mouse. In this manuscript we describe the function of the three human Aurora/Ipl1p-related kinases, and review the genomic alterations reported for the chromosome region where the kinase genes localise. But we first discuss the impact of the human genome sequence project for the identification of new kinases in the context of cancer research.
Aurora, Ipl1p Related Kinases, CDNA microarrays, Cellular apoptosis susceptibility, HsAIRK1, Xenopus laevis, HsAIRK2, HsAIRK3
CNRS UPR41, Universite de Rennes 1, CS 34317 Rennes Cedex France