Risk Factors for Lymph Node Metastasis in Undifferentiated-Type Gastric Carcinoma

Undifferentiated-type carcinoma has a high incidence of lymph node metastasis. The independent risk factors for lymph node metastasis in undifferentiated-type carcinoma are invasion depth, tumor size, lymphovascular invasion, and presence of ulcer. In the cases that meet the curative resection criteria, no lymph node metastasis was observed in the Japanese studies, but some metastases were observed in Korean studies. After performing curative endoscopic submucosal dissection, the survival rate is similar to that of gastrectomy. The discrepancy between endoscopy and pathology is high in undifferentiated-type carcinoma. The tumor size in endoscopy is a significant risk factor for non-curative resection, and when the tumor size is small, the non-curative resection rate is significantly reduced. Lymphovascular invasion can be assessed in pathologic examination and D2-40 stain is helpful. The presence of ulcer should be determined by pathology, but ulcer’s omission in pathology report makes the analysis difficult. Undifferentiatedtype carcinomas with differentiated-type components show higher lymph node metastasis rate than that of pure undifferentiatedtype carcinomas. The lymph node metastasis rate of signet ring cell type is lower than that of other undifferentiated-type carcinomas and is similar to differentiated-type carcinomas. The application of these additional histologic findings may improve the indication of endoscopic submucosal dissection

Chronic Pelvic Paragonimiasis: Radiological Findings

Two cases of ectopic paragonimiasis involving pelvic peritoneal cavity and omentum were confirmed surgically and pathologically, The lesions were manifested as nodules of faintly calcified periphery on various imaging modalities. Ectopic paragonimiasis should be included in the differential diagnosis of nodular calcifications in the pelvic cavity

A standardized pathology report for gastric cancer: 2nd edition

The first edition of ‘A Standardized Pathology Report for Gastric Cancer’ was initiated by the Gastrointestinal Pathology Study Group of the Korean Society of Pathologists and published 17 years ago. Since then, significant advances have been made in the pathologic diagnosis, molecular genetics, and management of gastric cancer (GC). To reflect those changes, a committee for publishing a second edition of the report was formed within the Gastrointestinal Pathology Study Group of the Korean Society of Pathologists. This second edition consists of two parts: standard data elements and conditional data elements. The standard data elements contain the basic pathologic findings and items necessary to predict the prognosis of GC patients, and they are adequate for routine surgical pathology service. Other diagnostic and prognostic factors relevant to adjuvant therapy, including molecular biomarkers, are classified as conditional data elements to allow each pathologist to selectively choose items appropriate to the environment in their institution. We trust that the standardized pathology report will be helpful for GC diagnosis and facilitate large-scale multidisciplinary collaborative studies

Effects of Interleukin-10 Polymorphisms, Helicobacter pylori Infection, and Smoking on the Risk of Noncardia Gastric Cancer

OBJECTIVE: Both variations in the interleukin-10 (IL10) gene and environmental factors are thought to influence inflammation and gastric carcinogenesis. Therefore, we investigated the associations between IL10 polymorphisms, Helicobacter pylori (H. pylori) infection, and smoking in noncardia gastric carcinogenesis in Koreans. METHODS: We genotyped three promoter polymorphisms (-1082A>G, -819T>C, and -592 A>C) of IL10 in a case-control study of 495 noncardia gastric cancer patients and 495 sex- and age-matched healthy controls. Multiple logistic regression models were used to detect the effects of IL10 polymorphisms, H. pylori infection, and smoking on the risk of gastric cancer, which was stratified by the histological type of gastric cancer. RESULTS: The IL10-819C and -592C alleles were found to have complete linkage disequilibrium, and all three IL10 polymorphisms were associated with an increased risk of intestinal-type noncardia gastric cancer. These associations were observed only in H. pylori-positive subjects and current smokers. A statistically significant interaction between the IL10-592 genotype and H. pylori infection on the risk of intestinal-type gastric cancer was observed (P for interaction  = 0.047). In addition, H. pylori-positive smokers who were carriers of either the IL10-1082G (OR [95% CI]  = 17.76 [6.17-51.06]) or the -592C (OR [95% CI]  = 8.37 [2.79-25.16]) allele had an increased risk of intestinal-type gastric cancer compared to H. pylori-negative nonsmokers homozygous for IL10-1082A and -592A, respectively. The interaction between the IL10-1082 polymorphism and the combined effects of H. pylori infection and smoking tended towards significance (P for interaction  = 0.080). CONCLUSIONS: Inflammation-related genetic variants may interact with H. pylori infection and smoking to increase the risk of noncardia gastric cancer, particularly the intestinal-type. These findings may be helpful in identifying individuals at an increased risk for developing noncardia gastric cancer

Mixed-type gastric cancer and its association with high-frequency CpG island hypermethylation

Gastric carcinoma (GC) is one of the human cancers in which promoter CpG island hypermethylation is frequently found. We used the MethyLight assay to evaluate the methylation status of 16 CpG island loci that are hypermethylated in GC. We analyzed the relationship between CpG island hypermethylation of these 16 genes and the clinicopathological features in 191 advanced GCs. A significant difference was observed between the number of methylated genes in Epstein-Barr virus (EBV)-negative and microsatellite instability (MSI)-negative GCs of different histological types (Lauren classification; P < 0.01). We found that mixed-type (MT) carcinomas, which have both diffuse-type (DT) and intestinal-type (IT) components, had more methylated genes (10.6) than either DT carcinomas (7.6 methylated genes) or IT carcinomas (6.7 methylated genes) (P < 0.001). This trend was also observed when EBV-positive or MSI-positive GCs were excluded from the analysis (9.2, 6.9, and 4.8; P < 0.001). When the IT and DT components were dissected from MT carcinomas and the methylation of these 16 genes was evaluated, both components had a number of methylated genes similar to MT carcinomas, (10.2 and 9.7, respectively), which was significantly higher than was found in IT and DT carcinomas (P < 0.05). These findings indicate that MT carcinoma is distinct from IT and DT carcinomas in its enhanced CpG island hypermethylation status and implicate the enhanced promoter CpG island hypermethylation in the histogenesis of MT carcinoma.Park SY, 2009, J PATHOL, V219, P410, DOI 10.1002/path.2596Yoo EJ, 2008, VIRCHOWS ARCH, V452, P515, DOI 10.1007/s00428-008-0596-7Zheng HC, 2008, VIRCHOWS ARCH, V452, P525, DOI 10.1007/s00428-007-0572-7Leung WK, 2008, LANCET ONCOL, V9, P279, DOI 10.1016/S1470-2045(08)70072-XKang GH, 2008, LAB INVEST, V88, P161, DOI 10.1038/labinvest.3700707Ogino S, 2008, J MOL DIAGN, V10, P13, DOI 10.2353/jmoldx.2008.070082Enomoto S, 2007, CANCER SCI, V98, P1853, DOI 10.1111/j.1349-7006.2007.00625.xWood LD, 2007, SCIENCE, V318, P1108, DOI 10.1126/science.1145720Schuebel KE, 2007, PLOS GENET, V3, P1709, DOI 10.1371/journal.pgen.0030157Ushijima T, 2007, J BIOCHEM MOL BIOL, V40, P142Schlesinger Y, 2007, NAT GENET, V39, P232, DOI 10.1038/ng1950Jass JR, 2007, HISTOPATHOLOGY, V50, P113, DOI 10.1111/j.1365-2559.2006.02549.xOgino S, 2006, AM J SURG PATHOL, V30, P1175Weisenberger DJ, 2006, NAT GENET, V38, P787, DOI 10.1038/ng1834Chang MS, 2006, CLIN CANCER RES, V12, P2995, DOI 10.1158/1078-0432.CCR-05-1601Ogino S, 2006, J MOL DIAGN, V8, P209, DOI 10.2353/jmoldx.2006.050135Kusano M, 2006, CANCER, V106, P1467, DOI 10.1002/cncr.21789Oue N, 2006, CANCER, V106, P1250, DOI 10.1002/cncr.21754Saxonov S, 2006, P NATL ACAD SCI USA, V103, P1412, DOI 10.1073/pnas.0510310103Crew KD, 2006, WORLD J GASTROENTERO, V12, P354Parkin DM, 2005, CA-CANCER J CLIN, V55, P74Suriano G, 2005, GENE CHROMOSOME CANC, V42, P238, DOI 10.1002/gcc.20135An CH, 2005, CLIN CANCER RES, V11, P656Henson DE, 2004, ARCH PATHOL LAB MED, V128, P765Kang GH, 2002, AM J PATHOL, V160, P787GREENE FL, 2002, B AM COLL SURG, V87, P13Young J, 2001, AM J PATHOL, V159, P2107Esteller M, 2001, CANCER RES, V61, P3225Grady WM, 2000, NAT GENET, V26, P16Chan AOO, 1999, J GASTROEN HEPATOL, V14, P1150Stadtlander CTKH, 1999, CARCINOGENESIS, V20, P2195, DOI 10.1093/carcin/20.12.2195Toyota M, 1999, P NATL ACAD SCI USA, V96, P8681Machado JC, 1999, LAB INVEST, V79, P459Tahara E, 1996, SEMIN ONCOL, V23, P307LAUREN P, 1965, ACTA PATHOL MIC SC, V64, P31

The Different Clinicopathological Features of Remnant Gastric Cancer Depending on Initial Disease of Partial Gastrectomy

Background: The incidence of gastric cancer increases in the remnant stomach after partial gastrectomy; however, its pathogenesis remains controversial. The clinicopathological features and immunohistochemical subtype were evaluated in patients with remnant gastric cancer considering the initial cause of partial gastrectomy. Methods: We categorized 59 cases of remnant gastric cancer who underwent curative surgery between 2001 and 2016 according to initial pathologies of benign (n = 24) or malignant (n = 35). Histological changes including pyloric metaplasia and intestinal metaplasia in the mucosa around the anastomosis site and the background mucosa of carcinomas were compared between the groups. Results: In the malignant group, the proportion of male patients was substantially lower, with a shorter interval. In background mucosa around the carcinomas, incidence of high-grade pyloric metaplasia was significantly higher in the benign group (13/20, 65.0% vs. 10/28, 35.7%), while high-grade intestinal metaplasia was only observed in the malignant group (0/20, 0% vs. 7/28, 25.0%). Conclusions: The cancers in the initial benign disease are mainly associated with pyloric metaplasia at the anastomosis site, reflecting reflux, but not with intestinal metaplasia. On the other hand, in the initial malignant disease group, intestinal metaplasia has an equally important role as reflux-associated pyloric metaplasia

Reduced expression of CD99 and functional disturbance in anencephalic cortical thymocytes

In a significant proportion of cases, anencephaly is associated with thymic enlargement, suggesting a possibility that anencephalic fetuses have a functional disturbance in thymocyte differentiation and development. In this report, we demonstrated that CD99 expression was consistently reduced in cortical thymocytes of all anencephalic fetuses. In addition, the CD99-dependent aggregation of immature cortical thymocytes was almost completely impaired and apoptosis of thymocytes was markedly reduced in several cases. These results are in agreement with previous findings that CD99 regulates the aggregation and apoptosis of various types of cells. These data strongly suggest that functional disturbance of thymocytes and thymic hyperplasia are related to the reduced expression of CD99 molecule in anencephalic fetuses