Aberrant expression of cell-cycle regulator cyclin DI in breast cancer is related to chromosomal genomic instability

Jia Chyi Lung, Jan Show Chu, Jyh Cherng Yu, Chung Tai Yue, Yen Li Lo, Chen Yang Shen*, Cheng-Wen Wu

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

37 Scopus citations


To account for the accumulation of genomic alterations required for tumor progression, it has been suggested that the genomes of cancer cells are unstable and that this instability results from defective mutators (the "mutator phenotype" theory). To examine the hypothesis that abnormal cell-cycle regulators act as the mutators contributing to genomic instability, the present study, based on primary tumor tissues from 71 patients with breast cancer, was performed to determine whether there was an association between aberrant expression of cell-cycle regulators (cyclin A, cyclin DI, cyclin E, RBI, p21, and p27) and chromosomal instability. Comparative genomic hybridization was used to measure chromosomal changes, reflecting genomic instability in individual tumors, whereas immunohistochemistry was used to detect aberrant expression of cell-cycle regulators. Overexpression of cyclin DI was found to be significantly correlated with increased chromosomal instability (defined as harboring more than 7 chromosomal changes), with 63% of tumors overexpressing and 27% of tumors not overexpressing, with cyclin DI showing chromosomal instability (P < 0.05). Interestingly, this relationship was independent of cell outgrowth (as detected by the proliferation marker Ki-67) and was particularly significant in tumors not expressing p27 or in tumors with detectable RBI. These results suggest that cyclin DI plays an alternative role in the regulation of genomic stability.

Original languageEnglish
Pages (from-to)276-284
Number of pages9
JournalGenes Chromosomes and Cancer
Issue number3
StatePublished - 4 Jun 2002

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