SUMMARY:Bone marrow transplantation (BMT) is an effective therapeutic strategy for leukaemic malignancies and depressed bone marrow following cancer. However, its side effects on kidneys have been reported. Some drugs and irradiation are also suggested to be nephrotoxic. It is well known that haemolytic uraemic syndrome (HUS) after BMT develops as late-onset BMT nephropathy. Cyclosporine A (CsA) is a possible cause. Radiation nephropathy shows changes that are similar to the histology of HUS. These findings suggest that endothelial damage is closely associated with the pathogenesis of post-BMT nephropathy. Recently, some patients have developed glomerulonephritis accompanied by graft-versus-host disease (GVHD) after BMT. In these patients immune deposits are found mainly in subepithelium and mesangium equal to those of secondary membranous glomerulonephritis. A murine experimental model of GVHD manifests similar symptoms and histological changes to those of actual patients and may suggest the pathogenesis of glomerulonephritis.

An 84-year-old man, who was being followed up after lobectomy for lung carcinoma, was referred for evaluation of a dilated main pancreatic duct (MPD) from the body to the tail. Endoscopic ultrasonography demonstrated a low-echo mass occupying the MPD from the body to the tail. Endoscopic retrograde pancreatography showed an occlusion of the MPD in the body, and brush cytology indicated malignant cells. Distal pancreatectomy was performed. Grossly, a white-yellow, irregular-shaped solid mass without macroscopic mucus filled the lumen of the MPD. Histologically, the mass consisted of a complex fusion of tubular glands with atypical nuclei, which did not have intracellular mucus and oncocytic cytoplasm. The tumor mass showed abrupt transition to the normal epithelium. Immunohistochemically the tumor cells were partially positive for mucin 1 (MUC1) and MUC6, and negative for MUC2, MUC5AC, and lipase. Unfortunately the patient died of brain metastasis from lung carcinoma 15 months later. A review of reported cases of intraductal tubular tumors of the pancreas showed that the present case involved characteristics and immunohistochemical staining pattern similar to those of intraductal tubular carcinoma, although it might not be described as a typical intraductal tubular carcinoma under the existing Japanese rules.

These are the first studies characterizing methylation abnormalities in AIP. AIP's inflammatory condition may be related to carcinogenesis. Further study will elucidate methylation abnormalities associated with carcinogenesis in AIP.

In order to investigate the role of macrophages in glomeruli in the progression of glomerular sclerosis, methyl-cellulose (MC) was administered intraperitoneally to Wistar rats, in addition to intravenous injection of anti-thy1-1 antibody. In this group of rats (Thy-1 + MC group), many macrophages infiltrated in the lytic mesangium accompanied by rupture of capillary loops at an early stage and stayed with abundant deposition of mesangial matrices until day 35, whereas the proliferative lesions following mesangiolysis almost vanished in the rats treated with anti-thy1-1 antibody alone (Thy-1 group). In immunostaining, matrix metalloproteinase (MMP)-9 was expressed along regenerating capillaries of the Thy-1 group and in extracapillary lesions of the Thy-1 + MC group after day 7. In gelatin zymography, the gelatinolytic band for MMP-9 was expressed much more strongly in the Thy-1 + MC group than in the Thy-1 group at day 3, but it was expressed a little more strongly in the Thy-1 group than in the Thy-1 + MC group at day 7. The bands for an active form of MMP-2 were more strongly expressed in the Thy-1 + MC group than in the Thy-1 group throughout the experimental period. These results suggest that persistent accumulation of macrophages in mesangium induces glomerular sclerosis through expression and activation of MMP.

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Abbreviations: CA19-9, carbohydrate antigen 19-9; CKAE1/ AE3, cytokeratin AE1 and AE3; CD3, cluster of differentiation 3; CD20, cluster of differentiation 20; HMB-45, human melanoma black 45; INI1, integrase interactor 1; LCNEC, large cell neuroendocrine carcinoma; MMR, mismatch repair; NET, neuroendocrine tumor; SCC, squamous cell carcinoma; SMARCB1, swi/snfrelated, matrix-associated, actin-dependent regulator of chromatin, subfamily B, member 1 Correspondence