Cell Line ; Humans ; MicroRNAs ; metabolism ; Stomach Neoplasms ; metabolism

Gastric cancer is caused by the interaction of genetic and environmental factors. MicroRNA (miRNA) is involved in many cellular processes including proliferation, differentiation, and apoptosis and plays an important role in pathogenesis of gastric cancer, as demonstrated in many recent studies from perspectives including miRNA profiling, reciprocal modulation between epigenetic and miRNA, and Helicobacter pylori infection. MiRNA is highly stabe in blood, and therefore non-invasive diagnosis of gastric cancer using circulating miRNA may be promising.
Helicobacter pylori ; Humans ; MicroRNAs ; metabolism ; Stomach Neoplasms ; genetics

Gastrectomy ; Humans ; MicroRNAs ; analysis ; Statistics as Topic ; Stomach Neoplasms ; genetics ; metabolism

We have occasionally experienced eosinophilic abscess of the liver in patients with gastric carcinoma, suggesting that some eosinophil mobilizing (chemotactic and proliferative) factors might be produced by carcinoma cells. The aim of this study was to determine whether or not gastric carcinoma expresses the well-known eosinophil chemotactic factors (ECFs) and whether or not the expression is related to the histologic subtypes. Seventeen consecutive surgically removed tumor-bearing stomachs were collected: 7 signet ring cell type, 7 poorly differentiated tubular adenocarcinoma, and 3 moderately differentiated tubular adenocarcinoma. Hematoxylin-eosin stained sections were re-evaluated for eosinophil and mast cell infiltration. The expression of IL-2, IL-5 and granulocyte-macrophage colony stimulating factor (GM-CSF) were examined by immunocytochemical stain. There was no available frozen tissue for IL-2 and IL-5 in one case. Gastric carcinoma expressed IL-2 in all 16 cases, IL-5 in 12 of 16 cases and GM-CSF in 10 of 17 cases. Of particular interest, 7 of 10 GM-CSF-expressing carcinomas were signet ring cell type. Even in the remaining 3 cases, most GM-CSF-positive cells were signet ring cells scattered within tubular adenocarcinoma. No correlation of ECF expression between either eosinophil/mast cell infiltration or peripheral blood eosinophilia was identified. In conclusion, most gastric carcinomas express the well-known ECFs and the expression of GM-CSF is specific for signet ring carcinoma cells.
Cell Movement/physiology ; Chemotactic Factors, Eosinophil/metabolism* ; Eosinophils/physiology ; Human ; Immunohistochemistry ; Mast Cells/physiology ; Stomach Neoplasms/physiopathology ; Stomach Neoplasms/pathology ; Stomach Neoplasms/metabolism*

Animals ; Colonic Neoplasms ; metabolism ; pathology ; Female ; Humans ; Liver Neoplasms ; metabolism ; secondary ; Lymphatic Metastasis ; Neoplasm Proteins ; metabolism ; Ovarian Neoplasms ; metabolism ; pathology ; Protein Tyrosine Phosphatases ; metabolism ; Stomach Neoplasms ; metabolism ; pathology

OBJECTIVETo analyze the clinicopathologic features and prognosis of α-fetoprotein (AFP)-producing gastric cancers (AFPGC).

METHODSFifty-one serum AFP-positive patients with positive immunohistochemical staining of AFP in the primary lesions (study group) and sixty-five gastric cancer cases with normal AFP level (control group) treated in our department from January 2005 to December 2007 were included in this study. Their clinicopathologic features and follow-up data were statistically analyzed.

RESULTSCompared with the control group, the study group had a higher incidence of poorly differentiated adenocarcinoma (P=0.021) and liver metastasis (P=0.001) than that in the control group.The TNM stages in the study group were significantly higher than those in the control group (P=0.001). The 1-, 2-, and 5-year survival rates of the study group were 62.7%, 27.5% and 4.7%, respectively, and the median survival was 16 months, significantly lower than the 84.6%, 55.4%, 16.5%, and 30 months of the control group (P<0.001 for all). The serum AFP levels in the study group ranged from 58.63 µg/L to 12 100.00 µg/L, and could be classified into two groups:27 cases <500 µg/L, and 24 cases ≥500 µg/L. There was no significant difference of the immunohistochemical staining results between the two subgroups (P=0.912).

CONCLUSIONSAFPGC is a special type of gastric cancer with high degree of malignancy and poor prognosis. Monitoring of serum AFP level can earlier detect the progression of disease and give corresponding treatment.

Adenocarcinoma ; Humans ; Incidence ; Liver Neoplasms ; Prognosis ; Stomach Neoplasms ; diagnosis ; metabolism ; pathology ; Survival Rate ; alpha-Fetoproteins ; metabolism

No abstract available.
Humans ; Peroxisome Proliferator-Activated Receptors/*metabolism ; Prostaglandin-Endoperoxide Synthase/*metabolism ; Stomach Neoplasms/*metabolism

Adenocarcinoma ; metabolism ; pathology ; Humans ; Stomach Neoplasms ; metabolism ; pathology ; alpha-Fetoproteins ; metabolism

Adolescent ; Catecholamines ; secretion ; Female ; Humans ; Lung Neoplasms ; diagnosis ; metabolism ; Paraganglioma, Extra-Adrenal ; diagnosis ; metabolism ; Stomach Neoplasms ; diagnosis ; metabolism

OBJECTIVETo investigate the expression of annexin I in esophageal squamous cell carcinoma (SCC) and carcinomas of other histological types in order to analyze the correlation between the expression of annexin I and carcinogenesis.

METHODSFirst, a set of tissue microarray was established, which consisted of SCC from the esophagus (208 cases), lung, larynx, cervix, and external genital organs; adenocarcinomas from the lung, stomach, colon and rectum, liver, pancreas, breast, thyroid and kidney with 30 cases in each group, meanwhile, the corresponding normal tissue was also obtained for control. Immunohistochemistry was used to detect the expression of annexin I in different types of carcinomas and the corresponding normal controls from different organs. The correlation between the expression of annexin I and the clinicopathological feature was analyzed and compared, which included age, gender, differentiation grade and lymph node metastasis.

RESULTSIt was found that the expression of annexin I was decreased in esophageal SCC, when compared with normal esophageal squamous epithelia (P < 0.001), the similarity was also found in SCC of the lung, larynx and cervix. However, though negative in normal epidermis, annexin I expression was detected in some cases with SCC from external genital organs. Annexin I was found to be overexpressed in adenocarcinomas of the lung, stomach, colon and rectum, liver, pancreas, breast, thyroid and kidney, particularly very strong expression of annexin I was seen in lung adenocarcinoma, uterine endometrioid adenocarcinoma and ovarian serous adenocarcinoma. Interestingly, it was found to be positive in all thyroid papillary carcinomas, but negative in all normal thyroid glands. However, annexin I expression was found to be negative in all hepatocellular carcinoma and normal hepatocytes; and it was only detected in myoepithelium of normal breast tissue, but not in ductal luminal cells, and rarely in infiltrating ductal adenocarcinoma. In SCC, annexin I expression was stronger in well differentiated ones than that in the poorly differentiated ones. However, contrasting with SCC, in the adenocarcinomas from different organs, annexin I expression was much stronger in poorly differentiated ones than that in the well differentiate ones, especially in the adenocarcinomas from stomach, colon and rectum, pancreas, ovarian and kidney.

CONCLUSIONAnnexin I expression is quite different among different types of carcinomas, and is correlated with histopathological type and differentiation grade. Further study is needed to investigate its role in the carcinogenesis.

Adenocarcinoma ; metabolism ; pathology ; Annexin A1 ; metabolism ; Carcinoma, Endometrioid ; metabolism ; pathology ; Carcinoma, Squamous Cell ; metabolism ; pathology ; Cell Differentiation ; Endometrial Neoplasms ; metabolism ; pathology ; Epithelium ; metabolism ; Esophageal Neoplasms ; metabolism ; pathology ; Esophagus ; metabolism ; Female ; Humans ; Immunohistochemistry ; Lung Neoplasms ; metabolism ; pathology ; Stomach Neoplasms ; metabolism ; pathology