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.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Ponce-Castañeda MV,Lee MH,Latres E,Polyak K,Lacombe L,Montgomery K,Mathew S,Krauter K,Sheinfeld J,Massague Jsubject
Has Abstract,Author List Incompletepub_date
1995-03-15 00:00:00pages
1211-4issue
6eissn
0008-5472issn
1538-7445journal_volume
55pub_type
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