Finally, it was concluded that the two compounds 5b and 5a have the most promising anti-cancer activity against human breast carcinoma (MCF7), and it is believed that the anticancer activities of these two compounds were due to being the most effective in the inhibition of a member of IAPs groups, leading to activation of p53 gene and the Caspase-3 dependent apoptosis.
The results of this study showed that the relationship of antioxidant vitamins with breast cancer does not differ according to the presence or absence of the p53 mutation.
Previously, it was reported that mutations in p53 might render tumor cells more sensitive to Plk1 inhibition; however, p53 mutations are uncommon in breast cancer.
Germline mutations in tumor suppressor genes BRCA1 and p53 are used to illustrate the magnitude of the ethnic differences for breast cancer that might arise from differences in inherited susceptibility.
We conducted a case-control study to determine the prevalence of the R337H mutation by sequencing TP53 exon 10 in 123 women with breast cancer and 223 age- and sex-matched control subjects from southern Brazil.
Appropriate combinations of conventional factors with nuclear p53 immunoreaction and c-erbB-2 amplification would help to identify highly aggressive node-positive breast carcinomas and would aid stratification of patient groups in randomized clinical trials of adjuvant systemic therapies.
Ovarian hyperstimulation induces centrosome amplification and aneuploid mammary tumors independently of alterations in p53 in a transgenic mouse model of breast cancer.
As a whole, our data represent a p53 mutation profile in breast cancer cell lines, providing a model for structural, functional and pharmacological studies on p53 in human cancer.
We sought to detect p53 single amino acid variant (SAAV) peptides in breast cancer tumor samples that have been previously subjected to sequencing analysis.
Association between polymorphisms of XRCC1, p53 and MDR1 genes, the expression of their protein products and prognostic significance in human breast cancer.
These findings indicate that the SNPs in P53BP1 and p53 jointly contribute to breast cancer risk, particularly ER (-) or PR (-) breast cancer, and the p53Arg72Pro polymorphism may serve as a risk modifier.
Molecular pathological analysis of the structure and expression of constituents of the p53 pathway is likely to have value in diagnosis, in prognostic assessment and, ultimately, in treatment of breast cancer.
The p53 gene, a putative tumor suppressor gene located at 17p13, was examined for aberrations to determine whether it is the target for the 17p LOH in breast cancer.
In this study we have analyzed mRNA expression of both wild-type and mutated p53 and its respective Deltap53 isoform in 88 tumor samples from breast cancer in relation to clinical parameters and molecular subgroups.
These results have implications for the stratification of breast cancer based on p53 function and may provide an alternate explanation for deregulated p53 signalling in breast cancer.
Advances in the understanding of the molecular mechanisms implicated in breast cancer progression have led to the identification of many potential therapeutic gene targets, such as Breast Cancer 1/2, phosphatidylinositol 3-kinase catalytic subunit alpha, and tumor protein 53.
The aim of this study was to examine and determine whether p53 codon 72 and PIN3 Ins16 bp may be associated with an increased risk for breast cancer in female patients from the northwest of Iran.