<症例>石灰化胃癌の1例

By upper gastrointestinal series, a 57 years-old woman was pointed out to have scattered calcifications along the greater curvature of the stomach. On computerized tomography, the calcifications distributed in the irregularly thickened gastric wall. With a diagnosis of calcified mucinous adenocarcinoma showing Borrmann type III, total gastrectomy with splenectomy was carried out. The characteristics of this lesion were briefly presented with a review of the literature.57歳女性の上部消化管透視において, 胃の大弯側に散在性の小斑点状の石灰化が指摘された. この石灰化は, 腹部コンビューター断層撮影では不規則に肥厚した胃壁内に存在した. ボールマン III 型の石灰化胃粘液腺癌の診断で胃全摘・脾摘を行った. 画像診断と肉眼標本によって石灰化を証明できた胃癌はまれであり, 本邦報告例では女性に多く, すべて進行癌であった. 腫瘍の粘液産生がこの石灰化に関与すると考えられている. また, 切除率や生存率がかなり低い疾患でもあり, 自験例も術後2年半で癌再発により死亡した. 文献的考察を加えて報告した

The HGF/Met/NF-κB Pathway Regulates RANKL Expression in Osteoblasts and Bone Marrow Stromal Cells

Multiple myeloma (MM)-induced bone disease occurs through hyperactivation of osteoclasts by several factors secreted by MM cells. MM cell-secreted factors induce osteoclast differentiation and activation via direct and indirect actions including enhanced expression of receptor activator of nuclear factor &kappa;B ligand (RANKL) in osteoblasts and bone marrow stromal cells (BMSCs). Hepatocyte growth factor (HGF) is elevated in MM patients and is associated with MM-induced bone disease, although the mechanism by which HGF promotes bone disease remains unclear. In the present study, we demonstrated that HGF induces RANKL expression in osteoblasts and BMSCs, and investigated the mechanism of induction. We found that HGF and MM cell supernatants induced RANKL expression in ST2 cells, MC3T3-E1 cells, and mouse BMSCs. In addition, HGF increased phosphorylation of Met and nuclear factor &kappa;B (NF-&kappa;B) in ST2 cells, MC3T3-E1 cells, or mouse BMSCs. Moreover, Met and NF-&kappa;B inhibitors suppressed HGF-induced RANKL expression in ST2 cells, MC3T3-E1 cells, and mouse BMSCs. These results indicated that HGF promotes RANKL expression in osteoblasts and BMSCs via the Met/NF-&kappa;B signaling pathway, and Met and NF-&kappa;B inhibitors suppressed HGF-induced RANKL expression. Our findings suggest that Met and NF-&kappa;B inhibitors are potentially useful in mitigating MM-induced bone disease in patients expressing high levels of HGF