Early Gastric Cancer Presenting Pyloric or Prepyloric Stenosis

Out of 390 patients with early gastric cancer (EGC) who underwent gastric resection between Jan. 1968 and Jul. 1987, four patients developed pyloric stenosis and one patient developed prepyloric stenosis. Macroscopic types of EGC were II c in three cases and II c + III in two cases. Histologic types were tubular adenocarcinoma in four patients, and poorly differentiated adenocarcinoma in one patient. Cancer existed just right on or immediately adjacent to the pyloric ring in all patients; and extended transversely to the gastric axis in four patients, and longitudinally in one patient. An associated open ulcer and/or ulcer scar in the cancer lesion was seen in four patients, and submucosal fibrosis in three patients to a variety of degree, both of which were thought to be greatly attributed to pyloric or prepyloric stenosis. A duodenal ulcer was not present in any patients

Two cases of orbital adenocarcinoma treated with heavy charged carbon particle irradiation

Background: Orbital adenocarcinoma is a relatively rare, primary orbital malignant epithelial tumor, and shares the poor prognosis of orbital adenoid cystic carcinoma.We report the cases of two patients with orbital adenocarcinoma who were treated with heavy charged carbon particle irradiation and followed up for more 6 years. Method: Two patients with orbital adenocarcinoma, 62 and 74 years old, received 57.6 GyE of heavy charged particle irradiation therapy. Results: In both cases, the size of the tumor gradually decreased after carbon ion irradiation therapy. No recurrences or metastasis of the tumor were found for more than 6 years. Conclusion: Orbital adenocarcinoma has a poor prognosis in general. Two patients with orbital adenocarcinoma were treated with heavy charged carbon particle irradiation therapy and had a relatively good outcome and good prognosis. We believe that heavy charged carbon particle irradiation therapy is a promising therapy for orbital adenoud cystic carcinoma and adenocarcinoma

GADD34 activates p53 and may have utility as a marker of atherosclerosis

We previously identified growth arrest and DNA-damage-inducible gene 34 (GADD34) as a marker of ischemic stroke. In the present study, serum levels of anti-GADD34 antibodies were found to be significantly higher in patients with acute ischemic stroke or chronic kidney disease compared to healthy donors. We then examined the biological function of GADD34 by transfection into U2OS human osteosarcoma and U87 human glioblastoma cells. Knockdown of GADD34 by siRNA resulted in enhanced cell proliferation, which was reversed by co-knockdown of MDM2. Luciferase reporter assays revealed that the transactivation ability of p53 enhanced by genotoxic anticancer drugs such as camptothecin and etoposide was further potentiated by enforced expression of GADD34 but attenuated by co-transfection with p53 shRNA expression plasmids. Western blotting demonstrated increased p53 protein levels after treatment with camptothecin, which was also potentiated by GADD34 but suppressed by GADD34 siRNA, ATM siRNA, and ATM inhibitor wortmannin. GADD34 levels also increased in response to treatment with camptothecin or adriamycin, and this increase was attenuated by MDM2 siRNA. Immunoprecipitation with anti-GADD34 antibody followed by Western blotting with anti-MDM2 antibodies indicated ubiquitination of GADD34 is mediated by MDM2. Accordingly, GADD34 may function as a ubiquitination decoy to reduce p53 ubiquitination and increase p53 protein levels. Increased neuronal cell death due to activation of p53 by GADD34 may account for the elevated serum levels of anti-GADD34 antibodies observed in patients with acute ischemic stroke