Mutations of the p53 gene are closely associated with malignant transformation under in vitro conditions and are the most common genetic alteration in human malignancy.
The finding of a lower proportion of positivity in dysplastic lesions, and absence of staining in benign tumours, suggests that p53 mutation may be involved in the progression towards invasive malignancy in human squamous skin lesions.
We also examined the p53 tumor suppressor gene in constitutional cells from both mother and child for the possible presence of a cancer-predisposing inherited mutation, but none was found.
Our results suggest that multiple factors are involved in this malignancy, and that the simultaneous over-expression of p53 and the presence of ras mutation may be related to the progression stage of laryngeal carcinoma.
These results suggest that, while the primary disease gene for kidney cancer appears to be on chromosome 3, abnormalities of p53 are common and may be involved in the progression of this malignancy.
Expression of p53 and c-myc was investigated and compared with cell proliferative activity in a series of 40 hepatocellular carcinomas (HCC), by means of enhanced immunohistochemistry. p53 expression was demonstrated in 5 out of 40 HCC (12.5%) with the incidence increasing in 5 out of 40 HCC (12.5%) with the incidence increasing in proportion to the histological grading of malignancy: thus, 0% of well-differentiated, 6.9% of moderately differentiated and 33.3% of poorly differentiated lesions were positive.
The evidence for trisomies of 17q with loss of 17p in some cases of neuroblastoma led us to consider whether p53 mutations might contribute to the onset and progression of this malignancy.
To establish a genetic model of the progression of head and neck squamous carcinoma we have defined the incidence and timing of p53 mutations in this type of cancer.
These observations highlight the critical role of p53 in the regulation of abnormal chromosome replication and afford an explanation for the association between p53 abnormalities, aneuploidy and biological aggression in cancer.
Mutations in the p53 tumor suppressor gene are the most common genetic alterations found in diverse types of human cancer, including the primary malignant brain tumor, glioblastoma multiforme.
Mutations affecting the p53 gene are associated with many human malignancies, but little is known about changes in p53 in unknown primary tumors (UPTs), which are characterized as tumors with advanced stages of malignancy.
Our results indicate that p53 protein is expressed in a number of central nervous system neoplasms, and suggest that in astrocytic tumors a possible association may exist between p53 protein expression and tumor progression through increasing histological grades of malignancy.
In this study, we show that this germ line Arg-Pro polymorphism at codon 72 of the p53 gene is associated with genetically determined susceptibility to smoking-induced lung cancer; a susceptible genotype Pro/Pro has a 1.7-fold higher risk of this cancer compared with other genotypes.
Mice lacking p53 are born normal but develop cancer after a lag of months, this suggests that p53 is not an initiating mutation in cancer, but probably a late event.