Nuclear-specific accumulation of () mRNA in promoter mutated follicular thyroid tumours visualised by in situ hybridisation: a possible clinical screening tool?

Aims: Upregulation of the () gene is a frequent finding in follicular thyroid carcinomas (FTCs) with metastatic features. The augmented expression is usually caused by promoter mutations. As TERT protein immunohistochemistry might not correlate to mRNA levels in follicular thyroid tumours, we therefore sought to determine if visualisation of mRNA through in situ hybridisation could highlight high-risk cases.

Proteomic Profiling of Diffuse Large B-Cell Lymphomas.

Objective: The aim of this study was to identify differences in proteome profiles of diffuse large B-cell lymphoma (DLBCL) of nongerminal center (non-GC) versus GC type in the search for new markers and drug targets.

Methods: Six DLBCL, with 3 repeats for each, were used for the initial study by proteomics: 3 non-GC and 3 GC DLBCL cases. For immunohistochemistry, tissue microarrays were made from 31 DLBCL samples: 16 non-GC de novo lymphomas and 15 GC cases (11 transformed from follicular lymphomas and 4 de novo GC lymphomas).

Maspin, a Marker of Serrated Colorectal Polyps.

The serine proteinase inhibitor maspin is a tumor-suppressor protein that stimulates apoptosis and inhibits motility, invasion and cancer metastasis. Mutant maspin galvanises partial loss of tumor-suppressor function, reducing susceptibility to apoptosis and facilitating malignant progression. Mutant maspin has been reported in many tumor types.

Maspin highlights colorectal serrated polyps: preliminary findings.

Aims: Maspin, a 42-kDa serine proteinase inhibitor, is a tumor suppressor protein that stimulates apoptosis and inhibits motility, invasion and cancer metastasis. Mutant maspin leads to partial loss of tumor suppressor function, decreased susceptibility to apoptosis and to malignant progression. We recently found maspin expression (ME) in the cytoplasm of serrated colonic lesions, such as hyperplastic polyps (HP) and sessile serrated adenoma/polyps (SSA/P).

β-catenin Helices in the cytoplasm of sporadic and FAP duodenal adenomas.

Background: Initiation and progression in conventional adenomas is triggered by deregulation of Wnt/β-catenin signaling. In the absence of Wnt signal (off-state), β-catenin prevents phosphorylation of glycogen synthase kinase (GSK)-3β leading to aberrant nuclear accumulation in human tumors. While investigating the nuclear expression of β-catenin in biopsies from duodenal adenomas, we observed a non-previously reported phenomenon, namely the presence of β-catenin cytoplasmic helices (coils).

β-catenin helices in the cytoplasm of sessile serrated adenoma/polyps and conventional colorectal adenomas.

Initiation and progression in conventional adenomas is triggered by deregulation of WNT/β-catenin signaling. In the absence of WNT signal (off-state), β-catenin prevents phosphorylation of GSK3β, leading to aberrant nuclear accumulation in human tumors. It has been postulated that mutations in the β-catenin gene are always associated with a morphologically-neoplastic course.

Paucity of synaptophysin-expressing cells in Barrett's mucosa.

Aims: To assess synaptophysin expression in columnar-lined oesophageal mucosa showing either goblet cells, known as intestinal metaplasia, or with accompanying oxyntic glands or pyloric glands.

Methods And Results: Of 159 biopsies, 53 were oesophageal (19 had intestinal metaplasia, 13 oxyntic glands, and 21 pyloric glands), 77 gastric (12 had goblet cells and 27 no goblet cells) and 29 duodenal. Synaptophysin-positive goblet cells were found in all biopsies from the normal duodenum, in 53% of the oesophageal biopsies showing intestinal metaplasia, but only in 8% of gastric biopsies showing intestinal metaplasia.

A method to assess the distribution and frequency of plasma cells and plasma cell precursors in autoimmune hepatitis.

Chronic inflammation exhibiting interface hepatitis and plasma cells in hematoxylin-eosin (H&E)-stained sections is typical of autoimmune hepatitis (AIH), a non-resolving inflammatory liver disease of unidentified cause. Some biopsies may only reveal lymphocytes and occasional granulocytes but no plasma cells. Recent studies on liver biopsies showed that the antibody against multiple myeloma oncogene-1 (MUM1) stained plasma cells (PC), and plasma cell precursors (PCP).