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Identification of additional complementation groups that regulate genomic instability
Author(s) -
Hall Ingrid J.,
Gioeli Dan,
Weissman Bernard E.,
Tlsty Thea D.
Publication year - 1997
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(199710)20:2<103::aid-gcc1>3.0.co;2-7
Subject(s) - complementation , biology , somatic cell , genetics , gene , phenotype , cell culture , genome instability , microbiology and biotechnology , gene duplication , cancer research , dna damage , dna
By somatic cell hybridization, amplification has been found to be a recessive genetic trait in three tumor cell lines examined. Studies with transgenic mice have shown that amplification frequency can be altered by a lack of wild‐type TP53 ( p53 ) activity. Other factors may regulate this phenotype in tumor cell lines possessing both wild‐type p53 activity and amplification ability. Complementation analysis of somatic cell hybrids was performed to delineate groups of tumor cell lines that share a common defect that modulates the ability to amplify. The amplification frequencies of three normal fibroblast × tumor hybrids were suppressed 10–100‐fold from parental tumor values, extending the observation that amplification is a recessive genetic characteristic in these cell lines. Analysis of tumor × tumor hybrids revealed at least two complementation groups. Defects in these groups differed from TP53 and implicate multiple variables in the regulation of gene amplification. Genes Chromosomes Cancer 20:103–112, 1997. © 1997 Wiley‐Liss, Inc.