CD30 antigen is a trans-membrane glycoprotein belonging to the tumor necrosis factor receptor superfamily.[1][1] Upon stimulation, CD30 exerts pleiotropic effects on cell growth and survival, which largely depend on the NF-κB pathway activation.[2][2] In normal or inflamed tissues, CD30 expression

Operative link for gastritis assessment vs operative link on intestinal metaplasia assessment

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Summary: Background: Among Western populations, the declining incidence of Helicobacter pylori infection coincides with a growing clinical impact of autoimmune gastritis.Aims: To describe the histological phenotype of autoimmune gastritis, also to test the prognostic impact of OLGA staging in the autoimmune setting.Methods: A single‐institutional series (spanning the years 2003–2011) of 562 consecutive patients (M:F ratio: 1:3.7; mean age = 57.6 ± 14.4 years) with serologically confirmed autoimmune gastritis underwent histology review and OLGA staging.Results: Helicobacter pylori infection was ascertained histologically in 44/562 cases (7.8%). Forty six biopsy sets (8.2%) featured OLGA stages III–IV; they included all four cases of incidental epithelial neoplasia (three intraepithelial and one invasive; three of these four cases had concomitant H. pylori infection). There were 230 (40.9%) and 139 (24.7%) cases, respectively, of linear and micro‐nodular enterochromaffin‐like cell hyperplasia; 19 (3.4%) type I carcinoids were detected. The series included 116 patients who underwent repeated endoscopy/biopsy sampling (mean time elapsing between the two procedures = 54 months; range 24–108). Paired histology showed a significant (P = 0.009) trend towards a stage progression [the stage increased in 25/116 cases (22%); it remained unchanged in 87/116 cases (75%)].Conclusions: In autoimmune gastritis, the cancer risk is restricted to high‐risk gastritis stages (III–IV), and is associated mainly with concomitant H. pylori infection. OLGA staging consistently depicts the time‐dependent organic progression of the autoimmune disease and provides key information for secondary gastric cancer prevention strategies.

Significance: The role of the microRNA (miR) 15/16 family in oncogenesis and tumor progression has been intensively studied. The miR-15a/16-1 cluster is extensively described in B-cell chronic lymphocytic leukemia, characterized by the deletion of the 13q14 locus. The role of the miR-15b/16-2 cluster on chromosome 3q25 is still far from being elucidated. Because miR-15a is highly similar to miR-15b and miR-16-1 is identical to miR-16-2, we generated miR-15b/16-2 knockout mice to better understand the cluster’s role in vivo. These knockout mice developed B-cell lymphomas by age 15–18 mo, modulating the CCND2 (Cyclin D2), CCND1 (Cyclin D1), and IGF1R (insulin-like growth factor 1 receptor) genes involved in proliferation and antiapoptotic pathways in mouse B cells. Our results suggest a tumor suppressor role for the miR-15b/16-2 cluster in animal models of B-cell lymphomas.

Barrett's esophagus (BE) is characterized by the native stratified squamous epithelium (N) lining the esophagus being replaced by a columnar epithelium with intestinal differentiation (Barrett's mucosa; BM). BM is considered as the main risk factor for esophageal adenocarcinoma (Barrett's adenocarcinoma; BAc). MicroRNAs (miRNAs) are a class of small noncoding RNAs that control gene expression by targeting messenger RNAs and they are reportedly dysregulated in BM. To test the hypothesis that a specific miRNA expression signature characterizes BM development and progression, we performed miRNA microarray analysis comparing native esophageal mucosa with all the phenotypic lesions seen in the Barrett's carcinogenic process. Specimens were collected from 14 BE patients who had undergone esophagectomy, including: 14 with N, 14 with BM, 7 with low‐grade intraepithelial neoplasia, 5 with high‐grade intra‐epithelial neoplasia and 11 with BAc. Microarray findings were further validated by quantitive real‐time polymerase chain reaction and in situ hybridization analyses using a different series of consecutive cases (162 biopsy samples and 5 esophagectomies) of histologically proven, long‐segment BE. We identified a miRNA signature of Barrett's carcinogenesis consisting of an increased expression of 6 miRNAs and a reduced expression of 7 miRNAs. To further support these results, we investigated target gene expression using the Oncomine database and/or immunohistochemical analysis. We found that target gene expression correlated significantly with miRNA dysregulation. Specific miRNAs are directly involved in BE progression to cancer. miRNA profiling significantly expands current knowledge on the molecular history of Barrett's carcinogenesis, also identifying molecular markers of cancer progression.