WT1 expression in endometrioid ovarian carcinoma with and without associated endometriosis

WT1 silencing by RNAi synergizes with chemotherapeutic agents and induces chemosensitization to doxorubicin and cisplatin in B16F10 murine melanoma cells

“…Our results, as well as those of other authors (15)(16)(17)(18)(19)(20), indicate that WT1 is important in cell proliferation in a large number of tumors. In addition, WT1 downregulation results in the inhibition of cell proliferation and apoptosis induction by caspase 3 expression and PARP cleavage, suggesting that WY1 plays a distinct role in B16F10 melanoma growth (5,37).…”

“…WT1 encodes a transcription factor with zinc finger motifs, which is involved in gonadal development, sexual differentiation, cell proliferation and apoptosis (12,13 is considered an oncogene rather than a tumor suppressor gene (14) because its high expression levels are associated with the development and progression of a number of neoplasias, such as leukemia, as well as solid tumors, including mesothelioma (15), breast (16), colon (17), ovarian (18) and lung (19) cancer, and melanoma (20). High WT1 mRNA expression levels have been correlated with a biologically aggressive phenotype that has been associated with a poor prognosis for leukemia (21) and sarcoma (22).…”

KRAS mutations in ovarian low-grade endometrioid adenocarcinoma: association with concurrent endometriosis

“…Recently, Banz et al [22] reported differences in gene profiling between endometriosis-associated and endometriosis-independent EC. Previously, we showed that although only a minority of low-grade EC expressed the Wilms tumor antigen WT1, none of the positive cases were related to endometriosis [23]. These data suggest that EC might develop by more than 1 pathway and that a subgroup of these tumors could arise via mechanisms unrelated to endometriosis, possibly originating directly from the ovarian surface epithelium or from other sites.…”

“…The following data were recorded for each case: patient age, maximum tumor size, tumor grade, tumor stage, concurrent or metachronous endometrial neoplasia, and presence of associated endometriosis. Tumor grading was performed using the FIGO criteria for uterine endometrioid adenocarcinoma except that cytologically low-grade spindle cell and/or sex cord-like elements were not considered to represent solid (nonglandular) growth [23]. Tumor stage (FIGO) was based on the results of the surgical and pathologic findings including, where relevant, additional information obtained at weekly gynecology oncology tumor conference meetings.…”

Immunophenotypic analysis of ovarian endometrioid adenocarcinoma: Correlation with KRAS mutation and the presence of endometriosis

“…11 In turn, nuclear b-catenin induces the up-regulation of several key mediators that exert cell cycle control including cyclin D1. 16 Banz et al reported differences in gene profiling between endometriosis associated and endometriosis independent OECs. Similarly, the majority of p53 mutations lead to stabilisation of the mutant p53 protein, and hence its nuclear immunoexpression, although some mutations are characterised by complete loss of staining.…”