Identification of additional complementation groups that regulate genomic instability
| Autor: | I J, Hall, D, Gioeli, B E, Weissman, T D, Tlsty |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Phosphonoacetic Acid
Antimetabolites Antineoplastic Aspartic Acid Cell Cycle Genetic Complementation Test Gene Amplification Genes Recessive Fibroblasts Hybrid Cells Genes p53 Drug Resistance Neoplasm Multienzyme Complexes Aspartate Carbamoyltransferase Tumor Cells Cultured Humans Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing) Dihydroorotase Tumor Stem Cell Assay |
| Zdroj: | Genes, chromosomescancer. 20(2) |
| ISSN: | 1045-2257 |
| Popis: | 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 x 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 x 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. |
| Databáze: | OpenAIRE |
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