AI Article Synopsis
- The study investigates the connection between genetic recombination and the loss of tumor suppressor genes, specifically focusing on p53 in solid tumors.
- Findings reveal that both alleles of the p53 gene were deleted and truncated due to a specific chromosomal translocation (t(17;20)) and a large genomic deletion on chromosome 17p.
- The research indicates that genetic instability can result in the inactivation of tumor suppressor genes, provides detailed mapping of a recombination event, and clarifies the orientation of the p53 gene on chromosome 17 as from the centromere to the telomere.
Article Abstract
Little is known about the relationship between genetic recombination mechanisms and loss of tumour suppressor genes in solid tumours. Here, we demonstrate deletion and truncation of both p53 alleles in a primary human glioblastoma and a derived cell line as the combined result of a t(17;20) reciprocal translocation and a 1.1 Mbp genomic deletion on chromosome 17p, starting in intron 4 of the p53 gene and ending at the telomeric CA-repeat marker D17S960. These results (i) suggest that genetic instability can lead to loss of tumour suppressor gene function in solid cancers, (ii) provide mapping of one such recombination event at the nucleotide level, and (iii) establish the orientation of the p53 gene on chromosome 17 as: centromere 5'-3'-telomere.
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| http://dx.doi.org/10.1038/sj.onc.1201544 | DOI Listing |
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