p27Kip1: chromosomal mapping to 12p12-12p13.1 and absence of mutations in human tumors. Academic Article uri icon

Overview

abstract

  • The p27Kip1 gene codes for a cyclin-dependent kinase inhibitor implicated in G1 arrest by transforming growth factor beta, cell-cell contact, agents that elevate cyclic AMP, and the growth-inhibitory drug rapamycin. p27 binds to and inhibits complexes formed by cyclin E-cdk2, cyclin A-cdk2, and cyclin D-cdk4. The involvement of p27 in the negative regulation of cell proliferation suggests that it may also function as a tumor suppressor gene. Using a combination of somatic cell hybrid panels and fluorescence in situ hybridization p27Kip1 has been mapped to the short arm of chromosome 12 at the 12p12-12p13.1 boundary, reported to harbor deletions and rearrangements in leukemia and mesotheliomas. In order to assess potential p27Kip1 gene alterations, we have screened a total of 147 human primary solid tumors and found no detectable cancer-specific mutations. These results argue that the often observed loss of antimitogenic transforming growth factor beta responsiveness in human cancer cells is not due to structural defects in p27Kip1.

publication date

  • March 15, 1995

Research

keywords

  • Chromosome Mapping
  • Chromosomes, Human, Pair 12
  • Cyclins
  • Mutation
  • Neoplasms
  • Protein Kinase Inhibitors

Identity

Scopus Document Identifier

  • 0028986932

PubMed ID

  • 7882310

Additional Document Info

volume

  • 55

issue

  • 6