Assessment of histologic risk factors for hepatocellular carcinoma in patients with chronic hepatitis B of advanced stage.

Histologic markers of increased risk for hepatocellular carcinoma can provide useful information for the management of patients with chronic hepatitis B. The expression of epithelial cell adhesion molecule (EpCAM, a marker of hepatic progenitor cells), p21 (a marker of hepatocyte senescence), glutamine synthetase (a marker of perivenular hepatocytes) and CD34 (a marker of sinusoidal capillarization) were assessed by immunohistochemistry in 52 liver biopsy specimens from patients with advanced stage chronic hepatitis B. Nineteen patients developed hepatocellular carcinoma during a follow-up period of 133 months. The findings were compared with those of 18 liver biopsy specimens from patients with early-stage chronic hepatitis B and 6 liver biopsy specimens without significant pathologic findings. EpCAM expression in hepatocytes was significantly increased in specimens with advanced stage, as compared with all other specimens. EpCAM positivity in over 30 % of hepatocytes was only seen in 3 specimens from patients who subsequently developed hepatocellular carcinoma. The expression of p21, glutamine synthetase and CD34 was not associated with hepatocellular carcinoma development. Nevertheless, glutamine synthetase immunostains highlighted zonality abnormalities that were useful in chronic hepatitis B staging. In conclusion, extensive immunopositivity of hepatocytes for EpCAM in chronic hepatitis B may represent a marker of increased hepatocellular carcinoma risk. Glutamine synthetase immunostaining represents a useful adjunct in determining the stage of chronic hepatitis B in diagnostic practice.

Systems-Level Mapping of Cancer Testis Antigen 1b/a to Sarcoma Pathways Identifies Activated Ran Binding-2 E3 SUMO-Protein Ligase and Transducin-Like Enhancer Protein 1.

Here we describe the identification of genes and their encoded proteins that are expressed in advanced grade tumors by reconstruction of a sarcoma cancer testis gene 1b/a (catg1b/a) network. CTAG1B/A is an ortholog of the yeast/Drosophila transcription factor Pcc1p, and a member of the KEOPS transcription complex. It has been implicated in telomere maintenance and transcriptional regulation through association with chromatin remodeling factors and is only expressed during adult testis germ cell differentiation. Ctag1b/a is re-activated in synovial sarcomas and myxoid liposarcomas but not in differentiated liposarcomas. We mapped CTAG1B/A protein to sarcoma transcription pathways with gene set expression analysis (GSEA) and using independent samples, we immunohistochemically identified expression of at least two network neighbors, RANBP2, and TLE1, thus validating our approach. This work demonstrates that mapping unknown genes to functional pathways by network re-construction is a powerful tool that can be used to identify candidate oncoproteins.

Combination of Adenomyoepithelioma and Adenoid Cystic Carcinoma of the Breast: A Case Report of an Uncommon Histopathological Entity.

BACKGROUND Adenomyoepithelioma and adenoid cystic carcinoma are uncommon types of breast tumors. Adenoid cystic carcinoma accounts for 0.1% of breast neoplasms and typically presents as a tender breast tumor, mostly in the subareolar area. Adenoid cystic carcinoma usually appears in women in the fifth or sixth decade of life and predominantly presents as a mixed tumor, with cribriform, tubular, and solid growth characteristics. Adenomyoepithelioma of the breast shows epithelial and smooth muscle characteristics. Adenomyoepithelioma rarely goes through malignant transformation and is an uncommon type of benign breast tumor. CASE REPORT Our study reviews the current published literature regarding the combination of these 2 rare neoplasms of the breast and shows a rare case of a 48-year-old woman with a combination of adenoid cystic carcinoma and adenomyoepithelioma. CONCLUSIONS The combination of adenoid cystic carcinoma and adenomyoepithelioma should be part of the differential diagnosis in breast cancer. More research is needed regarding the optimal therapy, which is currently surgical excision.

Concurrent presentation of nodal myeloid sarcoma and bone marrow chronic lymphocytic leukemia/small lymphocytic lymphoma: a unique association.

Myeloid sarcoma (MS), previously known as granulocytic sarcoma, is a rare, localized, tumor mass composed of myeloid precursor cells, with or without maturation, and occurring at an anatomical site other than the bone marrow (BM). Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), in contrast, is a B-cell hematological malignancy. We describe the first reported case of concurrent presentation of nodal MS and of BM CLL/SLL in the same patient. Fatal leukemic central nervous system infiltration was the final outcome. We provide possible explanations and investigate the pathophysiology of this unique, previously unreported co-morbidity.