作者: Jia-Chyi Lung , Jan-Show Chu , Jyh-Cherng Yu , Chung-Tai Yue , Yen-Li Lo
DOI: 10.1002/GCC.10072
关键词: Genetics 、 Comparative genomic hybridization 、 Genome instability 、 Cyclin E 、 Biology 、 Cyclin D 、 Cancer research 、 Cyclin A 、 Tumor progression 、 Cyclin D1 、 Chromosome instability
摘要: To account for the accumulation of genomic alterations required tumor progression, it has been suggested that genomes cancer cells are unstable and this instability results from defective mutators (the “mutator phenotype” theory). examine hypothesis abnormal cell-cycle regulators act as contributing to instability, present study, based on primary tissues 71 patients with breast cancer, was performed determine whether there an association between aberrant expression (cyclin A, cyclin D1, E, RB1, p21, p27) chromosomal instability. Comparative hybridization used measure changes, reflecting in individual tumors, whereas immunohistochemistry detect regulators. Overexpression D1 found be significantly correlated increased (defined harboring more than 7 changes), 63% tumors overexpressing 27% not overexpressing, showing (P < 0.05). Interestingly, relationship independent cell outgrowth (as detected by proliferation marker Ki-67) particularly significant expressing p27 or detectable RB1. These suggest plays alternative role regulation stability. © 2002 Wiley-Liss, Inc.