Objective: To examine the performance of the Risk of Malignancy Index (RMI) and Risk of Ovarian Malignancy Algorithm (ROMA) by histologic subtype and stage of disease in a cohort of women with ovarian cancer.
Methods: All patients with confirmed ovarian cancer at the Princess Margaret Hospital between February 2011 and January 2013 were eligible for study inclusion. Preoperative cancer antigen 125, human epididymis protein 4, and ultrasound findings were reviewed, and the sensitivity and false-negative rates of the RMI and ROMA were determined by stage of disease and tumor histology.
Objective: The brief Family History Questionnaire (bFHQ) was developed to identify endometrial cancer patients whose family histories suggest Lynch syndrome (LS). We compared the bFHQ, extended Family History Questionnaire (eFHQ) and dictated medical records (DMRs) to determine which family history screening strategy is superior in identifying LS in unselected women with newly diagnosed endometrial cancer that have undergone universal germline testing.
Methods: Prospective cohort study recruited women with newly diagnosed endometrial cancer to evaluate screening strategies to identify LS.
Background: Immunohistochemistry (IHC) for mismatch repair protein expression, microsatellite instability (MSI) testing, tumor morphology, and family history were compared to determine which screening strategy is superior in identifying Lynch syndrome (LS) in unselected women with newly diagnosed endometrial cancer (EC) who have undergone universal germline mutation testing.
Methods: A prospective cohort study was performed that recruited women with newly diagnosed EC. Participants completed a family history assessment with molecular characterization of EC with IHC and MSI testing and EC assessment for LS-associated morphologic features and underwent universal germline mutation testing for mutations in the mismatch repair pathway.
The transcription factor, Pax3, alters transcription by binding directly to promoter regions harbouring sequences recognized by either its paired domain or its homeodomain. We demonstrated previously that the promoter regions of many of the genes whose expression was altered during a Pax3-induced mesenchymal-to-epithelial transition harboured sequences recognized by lymphoid enhancer factor-1 (Lef1). Given the apparent lack of DNA-binding consensus sequences for Pax3 in these promoters, it was hypothesized that Pax3 might alter transcriptional activity of promoters harbouring Lef1-binding sites independent of Pax3 binding to DNA.
View Article and Find Full Text PDF