Concurrent amplification of cyclin E and CDK2 genes in colorectal carcinomas

Int J Cancer. 1995 Jul 4;62(1):25-8. doi: 10.1002/ijc.2910620107.

Abstract

The genetic changes of cyclin A, DI, E and CDK2 were examined in human colorectal carcinomas by Southern-blot analysis. Gene amplification of cyclin E was detected in 5 of 53 (9.4%) primary colorectal carcinoma tissues. Interestingly, in 3 of 5 tumors showing cyclin E gene amplification, the CDK2 gene was amplified simultaneously with rearrangements. No obvious correlation was detected between gene amplification and clinicopathological features of colorectal carcinomas. Out of 7 colon carcinoma cell lines, 2 showed gene amplification of cyclin E without gene amplification of CDK2. No amplification of cyclin A or DI gene was found in any of the colorectal carcinoma tissues or colon carcinoma cell lines. Our results suggest that the concurrent amplification of cyclin E and CDK2 genes may play a role in colorectal carcinogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • CDC2-CDC28 Kinases*
  • Colorectal Neoplasms / genetics*
  • Cyclin-Dependent Kinase 2
  • Cyclin-Dependent Kinases / genetics*
  • Cyclins / genetics*
  • Female
  • Gene Amplification*
  • Humans
  • Male
  • Protein Serine-Threonine Kinases / genetics*
  • Tumor Cells, Cultured

Substances

  • Cyclins
  • Protein Serine-Threonine Kinases
  • CDC2-CDC28 Kinases
  • CDK2 protein, human
  • Cyclin-Dependent Kinase 2
  • Cyclin-Dependent Kinases