PURPOSE: The p16 (MTS1) gene codes for a cyclin-dependent kinase inhibitor and may be a new tumor suppressor gene. It is frequently mutated in a variety of cell lines established from tumors. This is the first report of screening for alteration of the p16 gene in testicular, ovarian and endometrial malignancies. MATERIALS AND METHODS: We examined alterations of p16 in 78 primary genital tumors (42 testicular, 21 ovarian and 15 endometrial cancers) and mononuclear cells from 2 patients with Lynch syndrome II as well as 5 testicular tumor cell lines by single-strand conformation polymorphism (SSCP) and Southern blot hybridization. RESULTS: The DNA from the p16 gene of 2 testicular tumors (5%), an ovarian cancer (4%) and a testicular tumor cell line (20%) had altered migration in gel electrophoresis as shown by SSCP. Analysis of DNA sequence of these samples revealed a polymorphism at codon 140. Southern blot hybridization detected neither deletions nor rearrangements of the p16 gene in any of the samples. CONCLUSIONS: Taken together, these results suggest that p16 alterations probably are not important for tumorigenesis of testicular, ovarian and endometrial tumors.
PURPOSE: The p16 (MTS1) gene codes for a cyclin-dependent kinase inhibitor and may be a new tumor suppressor gene. It is frequently mutated in a variety of cell lines established from tumors. This is the first report of screening for alteration of the p16 gene in testicular, ovarian and endometrial malignancies. MATERIALS AND METHODS: We examined alterations of p16 in 78 primary genital tumors (42 testicular, 21 ovarian and 15 endometrial cancers) and mononuclear cells from 2 patients with Lynch syndrome II as well as 5 testicular tumor cell lines by single-strand conformation polymorphism (SSCP) and Southern blot hybridization. RESULTS: The DNA from the p16 gene of 2 testicular tumors (5%), an ovarian cancer (4%) and a testicular tumor cell line (20%) had altered migration in gel electrophoresis as shown by SSCP. Analysis of DNA sequence of these samples revealed a polymorphism at codon 140. Southern blot hybridization detected neither deletions nor rearrangements of the p16 gene in any of the samples. CONCLUSIONS: Taken together, these results suggest that p16 alterations probably are not important for tumorigenesis of testicular, ovarian and endometrial tumors.
Authors: P Chaubert; L Guillou; A M Kurt; M M Bertholet; G Metthez; H J Leisinger; F Bosman; P Shaw Journal: Am J Pathol Date: 1997-09 Impact factor: 4.307
Authors: Andrzej Semczuk; Carsten Boltze; Barbara Marzec; Anna Szczygielska; Albert Roessner; Regine Schneider-Stock Journal: J Cancer Res Clin Oncol Date: 2003-08-14 Impact factor: 4.553
Authors: R Nakashima; M Fujita; T Enomoto; T Haba; K Yoshino; H Wada; H Kurachi; M Sasaki; K Wakasa; M Inoue; G Buzard; Y Murata Journal: Br J Cancer Date: 1999-05 Impact factor: 7.640