p16 mutations/deletions are not frequent events in prostate cancer

Cyclin-dependent kinase-4 inhibitor gene (p16INK4) has recently been mapped to chromosome 9p21. Homozygous deletions of this gene have been found at high frequency in cell lines derived from different types of tumours. These findings suggested therefore, that p16INK4 is a tumour-suppressor gene invo...

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Bibliographic Details
Published in:British journal of cancer 1996-07, Vol.74 (1), p.120-122
Main Authors: Tamimi, Y, Bringuier, PP, Smit, F, van Bokhoven, A, Debruyne, FMJ, Schalken, JA
Format: Article
Language:English
Subjects:
Base Sequence
Biological and medical sciences
Biomedical and Life Sciences
Biomedicine
Cancer Research
Carrier Proteins - genetics
Cyclin-Dependent Kinase Inhibitor p16
Drug Resistance
Epidemiology
Exons
experimental-oncology
Gene Deletion
Humans
Male
Medical sciences
Molecular Medicine
Molecular Sequence Data
Mutation
Nephrology. Urinary tract diseases
Oncology
Polymerase Chain Reaction
Polymorphism, Single-Stranded Conformational
Prostatic Neoplasms - genetics
Tumor Cells, Cultured
Tumors of the urinary system
Urinary tract. Prostate gland
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Summary:Cyclin-dependent kinase-4 inhibitor gene (p16INK4) has recently been mapped to chromosome 9p21. Homozygous deletions of this gene have been found at high frequency in cell lines derived from different types of tumours. These findings suggested therefore, that p16INK4 is a tumour-suppressor gene involved in a wide variety of human cancers. To investigate the frequency of p16INK mutations/deletions in prostate cancer, we screened 20 primary prostate tumours and four established cell lines by polymerase chain reaction (PCR) and single-strand conformation polymorphism (SSCP) analysis for exon 1 and exon 2. In contrast to most previous reports, no homozygous deletions were found in prostate cancer cell lines, but one cell line (DU145) has revealed to a mutation at codon 76. Only two SSCP shifts were detected in primary tumours: one of them corresponds to a mutation at codon 55 and the other one probably corresponds to a polymorphism. These data suggest that mutation of the p16INK4 gene is not a frequent genetic alteration implicated in prostate cancer development.
ISSN:0007-0920
1532-1827
DOI:10.1038/bjc.1996.325