The TP53 gene, which encodes a DNA sequencedependent transcriptional regulator, is arguably the most frequently mutated gene in human cancer. Whereas wildtype p53 is restricted to its cognate DNA binding sites, mutant p53 (via mutation in the DNA binding domain) is no longer constrained to specific genomic sites. Mutant p53 proteins therefore cannot effectively mediate wildtype p53 tumor suppre...

Induction of WAF1 expression was investigated after heat treatment (44 degrees C, 30 min) in two human glioblastoma cell lines with the wild-type or a mutant p53 gene. WAF1 accumulation was induced by heat treatment in A-172 cells carrying the wild-type p53 gene but not in T98G cells carrying the mutant p53 gene. We examined whether this phenomenon was due to the induction of WAF1 expression. N...

BACKGROUND p53 plays a key role in the apoptotic event induced by chemotherapeutic agents. Mutation of p53 gene has been observed in various spontaneous tumors in humans and is associated with a poor prognosis. p53 abnormalities have been evaluated in several tumors in dogs; however, the association of p53 gene mutation with clinical outcome in dogs with lymphoma has not been documented. HYPO...

Coordinate loss of one copy of the p53 gene and mutation of the remaining copy occur in colorectal carcinomas and in many other human malignancies. However, the prevalence of p53 gene mutations in carci nomas which maintain both parental copies of p53 has not previously been evaluated. Moreover, it is not known whether p53 gene mutations are limited to malignant tumors or whether they can also ...

Cancer gene therapy strategies for inducing apoptosis in solid tumors may allow contemporary medicine to reassess its management of these cancers. We demonstrated previously that overexpression of the wild-type p53 gene in squamous cell carcinoma of the head and neck cell lines via adenovirus-mediated gene transfer suppressed growth both in vitro and in vivo. Here, we characterize the mechanism...

BACKGROUND The p53 protein function is essential for the maintenance of the nontumorigenic cell phenotype. Pancreatic tumor cells show a very high frequency of p53 mutation. To determine if restoration of wild type p53 function can be used to eliminate the tumorigenic phenotype in these cells, pancreatic tumor cell lines, PANC-1 and HTB80, differing in p53 status were stably transfected with ex...

The use of the tumor suppressor p53 for gene therapy of cancer is limited by the dominant negative inactivating effect of mutant endogenous p53 in cancer cells. We have shown previously that swapping the tetramerization domain (TD) of p53 with the coiled-coil (CC) from Bcr allows for our chimeric p53 (p53-CC) to evade hetero-oligomerization with endogenous mutant p53. This enhances the utility ...

p53, a tumor suppressor and a transcription factor, has been shown to transcriptionally activate the expression of a number of important genes involved in the regulation of cell growth, DNA damage, angiogenesis, and apoptosis. In a computer search for other potential p53 target genes, we identified a perfect p53 binding site in the promoter of the human type IV collagenase (also called 72-kDa g...

This study evaluated the transcriptional regulation of four reporter genes in Saccharomyces cerevisiae by the human tumor suppressor protein p53. The S. cerevisiae ADE2, HIS3 and URA3 genes were used with nutritional selections and the E. coli LacZ gene was used to quantitate reporter gene activation. DNA elements containing binding sites for p53 were introduced upstream of several 5' truncated...

We tested a population of over 60 patients with chronic myelogenous leukemia (CML) for changes in the structure and expression of the p53 gene, which is located on chromosome 17. Six of 27 (22%) blast crisis samples and 3 of 5 (60%) accelerated phase samples had rearrangements of chromosome 17, whereas only 3 of 42 (7%) chronic phase patients had cytogenetic changes in chromosome 17. There was ...