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Mutational analysis of the p21/WAF1/CIP1/SDI1 coding region in human tumor cell lines
Author(s) -
Terry Lori A.,
Boyd Jeff,
Alcorta David,
Lyon Tracy,
Solomon Greg,
Han Greg,
Berchuck Andrew,
Beach David,
Barrett J. Carl
Publication year - 1996
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/(sici)1098-2744(199608)16:4<221::aid-mc6>3.0.co;2-i
Subject(s) - biology , coding (social sciences) , human cell , computational biology , cell culture , cancer research , genetics , statistics , mathematics
p21/WAF1/CIP1/SDI1 is an important cell‐cycle mediator with tumor suppressor gene capabilities, and its inactivation could potentially lead to tumor progression. Because tumor suppressor genes are commonly inactivated by somatic and germline mutations, we analyzed a variety of human tumor cell lines for p21 mutations. We used single‐strand conformational analysis and direct sequencing to identify possible mutations in the p21 coding region. Two base‐alterations were observed in 41 immortalized human tumor cell lines. A previously reported polymorphism that results in a serine‐to‐arginine amino‐acid substitution at codon 31 was found in 24% (10 of 41) of the tumor cell lines but was also found in 10% (six of 62) of normal parental DNAs tested and 7% (three of 43) of normal DNAs from patients with primary endometrial tumors. Another nucleotide substitution found at codon 80 resulted in the replacement of threonine with methionine. Codon 80 changes were found in 7% (three of 41) of the tumor cell lines (all endometrial) and in 2% (one of 62) of the normal parental DNAs. (This article is a US Government work and, as such, is in the public domain in the United States of America.)