We conclude that gene expression patterns that distinguish omental metastasis from primary epithelial ovarian cancer can be identified and that many of the genes have functions that are biologically consistent with a role in oncogenesis, metastasis, and p53 gene networks.
This gene is one of the keys to clarifying the genetic etiology of epithelial ovarian cancer and particularly CCC, given the low incidence of p53 mutations in this tumor type.
High-grade serous ovarian cancer (HG-SOC), a major histologic type of epithelial ovarian cancer (EOC), is a poorly-characterized, heterogeneous and lethal disease where somatic mutations of TP53 are common and inherited loss-of-function mutations in BRCA1/2 predispose to cancer in 9.5-13% of EOC patients.
Because chemokine network is involved in OC progression, we evaluated associations between chemokine expression and survival in tumor suppressor protein p53 (<i>TP53</i>) wild-type (<i>TP53</i>WT) and mutant (<i>TP53</i>m) OC datasets.
We present the apparent BRCA1-related, although mutation negative, breast and ovarian cancer patient who subsequently was confirmed to be TP53 c.817C>T (p.R273C) mutation carrier and discuss the importance of peri-diagnostic oncogenetic TP53 testing in early breast cancer cases.
No correlation was found between p21 and p53 expression. p21 expression is a significant prognostic marker for improved survival in ovarian cancer and is associated with early FIGO stage and zero tumor residues after primary tumor resection.
Age-associated, low frequency TP53 mutations were also found in 100% of peripheral blood samples from 15 women with and without ovarian cancer (none with hematologic disorder).
Tissue sections and corresponding cyst and/or ascitic fluid cells from 79 patients with epithelial ovarian cancer were analyzed immunohistochemically for p53 expression.
In this study, we examined the mutational pattern of the p53 gene in 9 patients with epithelial ovarian cancers using tissue collected from different sites within the same patient.
Recently, this category of ovarian carcinoma has gained increasing attention owing to the recognition of morphological varieties of TP53-mutated high-grade ovarian carcinoma.
To determine the feasibility of mutant p53 as a molecular target for gene therapy in ovarian cancer, we constructed an adenovirus vector containing the wild-type p53 gene.
Our results indicated that the aberrations of the p53 gene were common in epithelial ovarian cancers and p53 aberration may occur late during ovarian cancer evolution.
We previously reported that targeting p53 for degradation by the human HPV E6 gene in the ovarian cancer cell line PA1 leads to an increase in the chemoresistant phenotype.