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ERβ expression is related to the severity of the disease, supporting the role of ERβ as a relevant biomarker of tumor progression and possible chemopreventive target in patients at risk of colonic neoplasia.

with a tendency to significance for myometrial invasion (P = 0.065) by univariate analysis (v 2 ) ( Table 1). Patients with a negative MTA3 immunohistochemical staining reaction showed better progression-free (P = 0.008), cause-specific (P < 0.001) and overall (P = 0.012) survival by univariate survival analysis ( Figure 3). Cox regression resulted in just one independent term that was predictive of progression-free survival, namely FIGO stage (P < 0.001). Independent prognostic factors for cause-specific survival were FIGO stage (P = 0.004), LVSI (P = 0.025), and MTA3 positivity (P = 0.001). Overall survival was also influenced only by FIGO stage (P < 0.001) ( Table 2).The data obtained revealed that MTA3 can be upregulated in human cancer cells and might contribute to a more aggressive phenotype. However, as only a few target genes of MTA3 have been identified, the consequence of MTA3 overexpression in human cancer cells is far from being understood. We here demonstrate for the first time that MTA3 is upregulated in advanced stages of uterine non-endometrial cancer, and is associated with FIGO surgical stage, lymph node involvement, and LVSI. In addition, MTA3 staining was associated with progression-free, cause-specific and overall survival of patients with non-endometrioid carcinomas. Overall, immunolabelling of MTA3 represents an independent prognostic factor for causespecific survival, suggesting that this antigen could be used as a simple and efficient parameter with which to identify high-risk patients.

In the present narrative review, we analyzed the relationship between seronegative celiac disease (SNCD) and immunoglobulin deficiencies. For this purpose, we conducted a literature search on the main medical databases. SNCD poses a diagnostic dilemma. Villous blunting, intraepithelial lymphocytes (IELs) count and gluten “challenge” are the most reliable markers. Immunohistochemistry/immunofluorescence tissue transglutaminase (tTG)-targeted mucosal immunoglobulin A (IgA) immune complexes in the intestinal mucosa of SNCD patients may be useful. In our experience, tTG-mRNA was similarly increased in seropositive celiac disease (CD) and suspected SNCD, and strongly correlated with the IELs count. This increase is found even in the IELs’ range of 15–25/100 enterocytes, suggesting that there may be a “grey zone” of gluten-related disorders. An immune deregulation (severely lacking B-cell differentiation) underlies the association of SNCD with immunoglobulin deficiencies. Therefore, CD may be linked to autoimmune disorders and immune deficits (common variable immunodeficiency (CVID)/IgA selective deficiency). CVID is a heterogeneous group of antibodies dysfunction, whose association with CD is demonstrated only by the response to a gluten-free diet (GFD). We hypothesized a familial inheritance between CD and CVID. Selective IgA deficiency, commonly associated with CD, accounts for IgA-tTG seronegativity. Selective IgM deficiency (sIgMD) is rare (<300 cases) and associated to CD in 5% of cases. We diagnosed SNCD in a patient affected by sIgMD using the tTG-mRNA assay. One-year GFD induced IgM restoration. This evidence, supporting a link between SNCD and immunoglobulin deficiencies, suggests that we should take a closer look at this association.