Hepatic Sinusoidal Obstruction Syndrome without Preceding Medical Events

Sinusoidal obstruction syndrome (SOS) is one of the severe complications of radiation, anticancer chemotherapy and immunosuppressive agents for transplantation. Autopsy of a case of rapidly progressive, uncontrollable severe ascites, without apparent signs of preceding drug toxicity, revealed a tensely enlarged liver and spleen, and 3000 ml of ascites attributed to secondary portal hypertension. Histopathological analysis disclosed sinusoidal endothelial damage and fibrous expansion from central veins. All the foregoing indicated hepatic SOS that needs to be included in the differential diagnosis of progressive ascites in patients without an apparent history of malignancy or transplantation.

Gastric adenocarcinoma arising in gastritis cystica profunda presenting with selective loss of KCNE2 expression

Gastritis cystica profunda(GCP) is a rare condition caused by ectopic entrapment of gastric glands,probably secondary to the disruption of muscularis mucosae.GCP is often associated with gastric adenocarcinoma,and loss of the KCNE2 subunit from potassium channel complexes is considered a common primary target molecule leads to both GCP and malignancy.In this study,we,for the first time,analyzed the expression of KCNE2 in surgically excised tissue from human gastric cancer associated with GCP and confirmed that reduced KCNE2 expression correlates with disease formation.

Cdx2 expression and its promoter methylation during metaplasia-dysplasia-carcinoma sequence in Barrett's esophagus

AIM:To examine how the expression of caudal type homebox transcription factor 2(Cdx2) is regulated in the development of malignancy in Barrett's esophagus.METHODS:Cdx2,mucin(MUC) series(MUC2,MUC5AC and MUC6),p53 and E-cadherin expression in Barrett's esophagus and adenocarcinoma specimens were examined by immunostaining.Isolated clusters of cells from(1) MUC2 and Cdx2-positive intestinal metaplastic mucosa;(2) MUC5AC and MUC6-positive,and MUC2 and Cdx2-negative high-grade dysplasia(HD),or intramucosal adenocarcinoma(IMC);and(3) MUC5AC,MUC6 and Cdx2-positive poorly-differentiated invasive adenocarcinoma(PDA) were analyzed by methylationspecific polymerase chain reaction using sets of primers for detecting methylation status of the Cdx2 gene.RESULTS:Most of the non-neoplastic Barrett's esophageal mucosa showing intestinal-type metaplasia with or without low-grade dysplasia was positive for E-cadherin,MUC series and Cdx2,but negative for p53.A portion of the low-grade to HD was positive for E-cadherin,MUC5AC,MUC6 and p53,but negative for MUC2 and Cdx2.The definite IMC area was strongly positive for MUC5AC,MUC6 and p53,but negative for MUC2 and Cdx2.Methylation of the Cdx2 promoter was not observed in intestinal metaplasia,while hypermethylation of part of its promoter was observed in hot dipped and IMC.Hypermethylation of a large fraction of the Cdx2 promoter was observed in PDA.CONCLUSION:Cdx2 expression is restored irrespective of the methylation status of its promoter.Apparent positive immunohistochemical results can be a molecular mark for gene silencing memory.

Primary Malignant Lymphoma of Prostate with Silent <i>MYD</i>88 Mutation

We present a case of primary malignant lymphoma of the prostate in a 77-year-old Japanese man. Immunohistochemical examinations revealed the presence of a non-GCB subtype of DLBCL (CD10 (-), Bcl-6 (-), MUM1 (+)), and genetic analysis disclosed a lack of typical codon 206 or 265 missense mutation in MYD88, suggesting that the case was of type3 (non-GCB andnon-ABC), a subtype of DLBCL. Three courses of chemotherapy (rituximab in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP)) were effective, and the patient has been free of the disease with no local or systemic recurrence for three years. Although the significance of silent mutation at hot spot of the highly oncogenic MYD88 gene in this case is unclear, a minute increase in translational efficiency by silent mutation may have contributed to the activation of MYD88.