자궁경부암에서의 cyclin D1 및 E의 발현

Abstract

Multiple genetic changes occur during the evolution of normal cells into cancer cells. Recent work has identified another category of genes that, when mutated, increase genetic instability and accelerate cellular evolution. These genes encode components of cell cycle checkpoints, which are positions of control that ensure the order of events in the cell cycle. And several checkpoints are regulated by a family of protein kinases, the CDKs, and their obligate activating partners, the cyclins. One of the most important checkpoint is in late G1, at which the cell commit itself to another round of DNA replication and at which both positive and negative external signals are integrated into the cell cycle. Many checkpoints are deregulated in oncogenesis, and this is often due to changes in cyclin-CDK complexes. Consequently, cell growth and division to become insensitive to external cues. G1 cyclins, cyclin D1 and E, together with a cdk partner, are believed to regulate cell cycle progression from G1 into S phase by modulating the activity of their substrates. In these studies, we examined for HPV types 16 and 18 by polymerase chain reaction (PCR) and for the accumulation of cyclin D1 and E by immunohistochemistry in 94 cases of cervical tissues. Cyclin index (CI) was defined as the percentage of positively labeled nuclei per 1000 cells. We found cyclin D1 and E expression was significantly low in HPV-positive cases. Other clinicopathologic prognostic factors were not correlated with cyclin D1 and E expression. Further study based on larger numbers of cases with correlation of cyclin D1 and E status and survival data will be necessary to examine the potential use of cyclin expression as a prognostic marker.