Women with heterozygous germline mutations in the BRCA1 tumour suppressor gene are strongly predisposed to developing early-onset breast cancer through loss of the remaining wild-type BRCA1 allele and inactivation of TP53.
Within the patient group with p53-negative tumors, TP53 rare homozygous (CC) carriers had a worse survival than G-allele (GG/GC) carriers; actuarial breast cancer-specific survival 71% versus 80%, P = 0.07; HR 1.8 (1.1 to 3.1), P = 0.03.
Whole genome analysis identified that a TP53 gene mutation exists in ER-positive breast cancers, although the frequency of TP53 gene mutation in luminal tumors is lower compared with basal-like or human epidermal growth factor receptor type 2 (HER2)-positive breast cancers.
While previous reports on breast cancers indicate that Caucasian women have a low frequency of p53 mutations, higher frequencies of mutations are reported in some Japanese populations.
While mouse double minute (MDM)2 or MDMX protein overexpression (often due to gene amplifications) may inactivate p53 in different tumour forms, so far, there is no evidence for MDM2 amplifications in breast cancers resistant to anthracyclines.
While a detailed understanding of p53 protein-mediated responses in normal breast tissues remains elusive, p53 appears to have a pivotal role in the effects of gamma radiation on normal breast epithelium, but not stromal cells, which may account for the differing clinical effects of gamma radiation in women treated for breast cancer.
While TP53 mutation and MYC amplification were synergistic in promoting tumor progression, PIK3CA mutation was found to have alleviated the oncogenic effect of either the TP53 mutation or MYC amplification, and was associated with a significant reduction in mitotic activity in TP53 mutated and/or MYC amplified breast cancer.
Whereas 40% of human breast carcinomas harbor mutations in the tumor suppressor protein p53, the use of tests demonstrating the presence of p53 mutations as a prognostic marker in breast cancer has not altered clinical management.
When BRCA1/2 BCs were compared to triple-negative (TN) sporadic tumours of the studied DDR proteins, BARD1 (p < 0.001), PARP1 (non-cleaved) (p < 0.001), and P53 (p = 0.002) remained significantly different in BRCA1/2 tumours compared with TN BC.
When all the eligible studies of codon 72 polymorphism were pooled into this meta-analysis, there was no evidence of significant association between breast cancer risk and p53 codon 72 polymorphism in any genetic model.
We transfected p21 and p53 tumor suppressor plasmids, into different breast cancer cell lines using inorganic nanoparticles (NPs) of carbonate apatite to evaluate the effect of gene expression on reducing breast cancer cell growth.
We therefore tested the hypothesis that taxanes confer a greater advantage than do anthracyclines on breast cancers with mutated TP53 than in those with wild-type TP53.
We therefore investigated the effect of TP53R72P and MDM2 SNP309 on breast cancer risk and age at onset of breast cancer in a pooled series of 5,191 cases and 3,834 controls from the Breast Cancer Association Consortium (BCAC).
We therefore conclude that mutations in exons 5-7 of p53 gene are rare causes of breast cancer among Bengalee Hindu caste females, and therefore of little help for genetic counseling and diagnostic purposes.
We tested seven polymorphisms in DNA repair genes XRCC1, ERCC2, XRCC3, XRCC2, EXOI and TP53 for a possible association with breast cancer risk in a sample of 672 case and 672 control Russian women.
We studied the biological characteristics of these tumours by comparing the overexpression of oncogenes ERBB2, MYC, CCND1 and RHOC and TP53 gene mutation rates in IBC with those found in locally advanced and not otherwise specified breast cancers.
We sought to determine whether expression of wtp53 protein, or conversion of endogenous mutant p53 (mtp53) into a functional p53 protein with small molecule PRIMA-1, can override the tumor-promoting effects of naturally occurring mtp53 protein in hormone-responsive T47-D human breast cancer cells.