Approximately half of all colorectal cancers show p53 (TP53) gene mutations, with higher frequencies observed in distal colon and rectal tumors and lower frequencies in proximal tumors and those with the microsatellite instability or methylator phenotypes. Alterations to this gene appear to have lit
TP53 mutations in human skin cancers
β Scribed by Giuseppina Giglia-Mari; Alain Sarasin
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 444 KB
- Volume
- 21
- Category
- Article
- ISSN
- 1059-7794
No coin nor oath required. For personal study only.
β¦ Synopsis
The p53 gene (TP53) is mutated in numerous human cancers. We have used it as a molecular target to characterize the induction of mutations in human skin cancers. About 50% of all skin cancers in normal individuals exhibit p53 mutations. This frequency rises to 90% in skin cancers of patients with the DNA-repair deficiency known as xeroderma pigmentosum (XP). These mutations are characterized by a specific signature, attributed to the ultraviolet uvB part of the solar spectrum. In this review, we will describe different p53 mutation spectra, in relation to the various histopathological types of skin cancers such as basal cell carcinoma (BCC), squamous cell carcinoma (SCC), and malignant melanoma as well as to the DNA repair efficiency of the patients. In particular, different mutational hot spots are found among the various spectra. We have tried to elucidate them in terms of induced DNA lesion hot spots, as well as speed of local nucleotide excision repair (NER) or sequence effects. The molecular analysis of these mutagenic characteristics should help in the understanding of the origin of human skin cancers in the general population.
π SIMILAR VOLUMES
Based on gene sequence homologies, a p53 (TP53) gene family become apparent with the addition of the most recently identified p63 (TP73L; formerly TP63) and p73 (TP73) genes to the already known p53. The p53 gene encodes for a unique protein eliciting well-known tumor suppressor gene (TSG) propertie
Manipulation of the mouse genome allows emulation of the genetic defects that give rise to human cancers and evaluation of the cooperating nature of different mutations in the transformation of distinct cell types. Here we review the generation of mice with specific missense mutations in p53 (TP53)
Analysis of the literature reporting p53 mutations shows that 8% of report display typographical mistakes with a notable increase in recent years. These errors are sometimes isolated, but in some cases, they concern several or even all mutations described in a single article. Furthermore, some works
Mutation in p53 (TP53) remains one of the most commonly described genetic events in human neoplasia. The occurrence of mutations is somewhat less common in sporadic breast carcinomas than in other cancers, with an overall frequency of about 20%. There is, however, evidence that p53 is mutated at a s
A detailed analysis of p53 (TP53) mutations involving the 42 CpG dinucleotides was performed to gain greater insight into the mutational mechanism leading to specific selection of these mutations. Although the majority of these CpG dinucleotides have been found to be mutated in cancer cells, the het