Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024623 (gastric cancer)
36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We detect the expression of epidermal growth factor (EGF) and epidermal growth factor receptor (EGFR) in 104 specimens of gastric cancer by avidin biotin-peroxides complex technique (ABC). The positive rates of EGF, EGFR and synchronous EGF and EGFR were 35.6%, 42.3%, 30.8% respectively. The positive expression of EGF and EGFR to gastric cancer tissue was inclined to occur in patients who were in advanced stages, of poorly-differentiated types, Borrmann III, IV types, scirrhous type, seroinvasive type or lymph node metastasic types. The survival rates at 1, 3, 5 years after gastrectomy in the patients with expression of EGF were significantly lower than the survival rates of the patients with negative expression (P < 0.05). The patients with synchronous expression of EGF and EGFR had the worst prognosis. After gastrectomy, all of them died within 4 years. It is indicated that EGF and EGFR could serve as biological indicators of gastric cancer malignancy and an index for evaluating, the prognosis of the patients with gastric cancer.
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PMID:[Clinical study on epidermal growth factor and its receptor in human gastric cancer]. 798 13

Effect of epidermal growth factor (EGF) on ornithine decarboxylase (ODC) was examined in human gastric cancer-derived KATO-III cells, because 125I-EGF binding studies indicated a presence of specific binding sites for EGF on these cells. Upon stimulation with EGF, both ODC mRNA expression and ODC enzyme activity were significantly increased in KATO-III cells. However, unlike in other cellular systems, both EGF-induced ODC mRNA expression and ODC enzyme activation were biphasic with the peaks at 15 +/- 10 min and 2.1 +/- 1.5 hrs (mean +/- SE) for mRNA, and 3.1 +/- 1.5 and 7.7 +/- 1.8 hrs (mean +/- SE) for enzyme activity, respectively. Therefore, KATO-III cell line may provide a unique model for the biochemical analysis of EGF action on ODC activation.
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PMID:Epidermal growth factor induces biphasic activation of ornithine decarboxylase in human stomach-derived KATO-III cells. 819 4

To evaluate the importance of epidermal growth factor receptors (EGFR) in the growth and progression of human gastric cancer, we immunohistochemically stained EGFR in specimens of gastric cancer and compared the results with histopathological findings. Fresh frozen sections obtained from 65 cases of gastric cancer were stained by indirect immunostaining technique using Oncogene Scince Inc. Cat. No. GR01 (528 IgG reported by Kawamoto et al.) as anti-EGFR monoclonal antibody. Of the 65 cases of gastric cancer, 17 (26.2%) were EGFR-positive. In differentiated cancer, EGFR was positive in 15 of 28 cases (53.6%) of advanced cancer, and 1 of 14 (7.1%) of early stage cancer. In undifferentiated cancer, 1 of 15 cases (6.7%) of advanced cancer was positive, but all 8 cases of early stage cancer were negative. In differentiated cancer, EGFR was more frequently positive in cases of advanced cancer than in those of early stage cancer (p < 0.05). These results suggest that EGFR are expressed or increase in the transition process from early to advanced stage cancer in differentiated gastric cancer. In addition, the lower EGFR-positive rate in cases of undifferentiated cancer than in those of differentiated cancer suggests that an increase in EGFR is not needed for cancer growth in most cases of undifferentiated cancer.
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PMID:[Immunohistochemical and histopathological study of expression of epidermal growth factor receptors in gastric cancer]. 827 61

The expression of epidermal growth factor (EGF) was immuno-histochemically examined in the primary lesions of 201 patients with advanced gastric cancer who underwent curative resection. EGF-positive tumor cells were detected in the specimens of 75 patients (37.3%). A significant correlation was observed between the extent of lymph node metastasis and EGF expression (p < 0.01), indicating that EGF-positive cancer has a tendency to lymph node metastasis. The 2-year and 5-year survival rates of the patients with EGF-negative tumors were 77.2% and 63.0%, respectively, while those with EGF-positive tumors were 59.1% and 47.5% respectively. The difference in survival rates reached a maximum 2 years after surgery, indicating that the patients with EGF-positive gastric cancer had a higher risk of early recurrence. Therefore, the amount of EGF produced by a tumor may play some role in the growth of metastatic tumors and residual tumor cells after surgery, and thus be a potential risk factor in recurrence.
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PMID:Epidermal growth factor in gastric carcinoma as a risk factor of postoperative recurrence. 827 39

A novel cell line called Trioma, which can proliferate and secrete a human monoclonal antibody in the basal medium, was established. Trioma was generated by somatic cell hybridization with human x human hybridoma and A431c, which is a cell line able to grow autonomously in the basal medium. A Trioma called TriH8 has been kept growing in the DMEM/F-12 medium for over 1 year and stably producing stomach cancer-reactive human IgM into culture medium at 10 micrograms/ml. TriH8 has a characteristic cytological phenotype, that is, to diminish cell growth in the presence of epidermal growth factor.
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PMID:Generation of somatic cell hybrids capable of proliferating and secreting human monoclonal antibody without any growth factor supplements. 843 53

Heparin-binding epidermal growth factor (EGF)-like growth factor (HB-EGF) is a member of the EGF family of polypeptide growth factors, which includes EGF, transforming growth factor alpha(TGF-alpha), amphiregulin (AR) and betacellulin (BTC). To assess the potential role of HB-EGF in human gastric carcinomas, the expression of HB-EGF and EGF receptor (EGF-R) was examined in normal and cancerous gastric tissues and cultured gastric cancer cell lines. By Northern blot analysis, there was a 4.7-fold increase in HB-EGF mRNA levels in human gastric cancers compared with normal gastric tissues. There was a concomitant 3.9-fold increase in EGF-R mRNA levels in these cancers. Immunostaining revealed co-localization in 72% of the cancer cells of HB-EGF and EGF-R. AR and BTC moieties were not evident by Northern blot analysis. However, using PCR, both AR and BTC mRNA species were demonstrated in normal and cancerous gastric tissues. By Northern blot analysis, HB-EGF, TGF-alpha, AR, BTC and EGF-R mRNA moieties were co-expressed in KATO III and NCI-N87 gastric cancer cell lines. Furthermore, HB-EGF, EGF and TGF-alpha enhanced the growth of both cell lines in a dose-dependent manner. Our findings suggest that HB-EGF is relatively abundant in human gastric cancers and that co-expression of the EGF ligand family may lead to excessive activation of EGF-R in this disorder.
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PMID:Co-expression of heparin-binding EGF-like growth factor and related peptides in human gastric carcinoma. 862 Dec 50

Alterations in the structure and function of oncogenes and tumor suppressor genes, as well as genetic instability at several other genetic foci may be responsible for stomach carcinogenesis. The particular combination of multiple gene changes found in gastric cancer differs depending on the two histological types, strongly indicating that different genetic pathways exist for well differentiated or intestinal type and poorly differentiated or diffuse type gastric cancers. In general, genetic instability, telomerase activity, CD44 abnormal transcripts, and p53 mutation, all of which are common events of two types of gastric cancer, may be involved mainly in the early stage of stomach carcinogenesis, whereas activation of oncogenes and overexpression of the epidermal growth factor-related growth factor system may chiefly confer progression on gastric cancer. A new strategy of molecular diagnosis of gastrointestinal cancer, which has been implemented as a routine service in the Hiroshima University Clinical Laboratory, may provide new opportunities for early cancer diagnosis and more accurate evaluation of prognosis or grade of malignancy.
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PMID:Molecular biological observations in gastric cancer. 865 14

Scirrhous gastric cancer cells proliferate rapidly with fibrosis, when the cancer cells invade into the submucosa of the stomach. To investigate the mechanisms responsible for the rapid proliferation, the growth interaction between gastric cancer cells and fibroblasts was examined. Human gastric cancer cell lines established from scirrhous carcinoma or well-differentiated adenocarcinoma were used. Human fibroblast cell lines were obtained from various organs. The growth interaction between gastric cancer cells and fibroblasts was examined by calculating the number of cancer cells or by measuring [3H]thymidine incorporation of cancer cells. Gastric fibroblasts specifically stimulated the growth of scirrhous gastric cancer cells, but not that of well-differentiated adenocarcinoma cells. The growth factor(s) produced from gastric fibroblasts were then partially purified and characterised. The growth-promoting factor(s) had apparent molecular weights of 10000 dalton and was sensitive both to heat and proteinase treatment. No inhibition for the factor(s) was achieved with defined anti-growth factor antibodies. In this study, differential responses of scirrhous and well-differentiated gastric cancer cells to orthotopic fibroblasts were shown. Rapid proliferation of scirrhous gastric carcinoma should be partly controlled by orthotopic fibroblasts. The growth factor(s) from gastric fibroblasts, which was distinct from various defined growth factors such as epidermal growth factor (EGF), basic fibroblast growth factor (b-FGF), transforming growth factor-alpha (TGF-alpha), keratinocyte growth factor (KGF), vascular endothelial growth factor (VEGF), insulin-like growth factor I (IGF-I), hepatocyte growth factor (HGF), platelet-derived growth factor (PDGF) and transforming growth factor beta 1 (TGF-beta 1) may play an important role in the progression of scirrhous gastric cancer cells.
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PMID:Differential responses of scirrhous and well-differentiated gastric cancer cells to orthotopic fibroblasts. 885 81

Expression of mRNA for heregulin (HRG), a member of the epidermal growth factor (EGF) family and its receptors, ErbB-3 and ErbB-4, were evaluated in human upper gastrointestinal (GI) mucosa. Multi-target reverse-transcriptase polymerase chain reaction (RT-PCR) analysis using capillary electrophoresis and laser-induced fluorescence allowed us to quantify the minute amounts of mRNA from one biopsy specimen with high sensitivity. HRG, ErbB-3 and ErbB-4 mRNA were detected in esophagus, stomach and duodenum and the highest expression was found in duodenum. In gastric cancer, mRNA for ErbB-4 was significantly overexpressed. Immunoreactivity of ErbB-4 in carcinoma cell membrane was also confirmed. These findings suggest that HRG and its receptors, ErbB-3 and ErbB-4 may be physiologically significant in the human upper GI mucosa, especially in duodenum, and that ErbB-4 may contribute to the growth of gastric cancer.
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PMID:Expression of mRNA for heregulin and its receptor, ErbB-3 and ErbB-4, in human upper gastrointestinal mucosa. 971 81

Rebamipide, a gastroprotective drug, is a compound selected from over 500 amino acid analogs of 2(1H)-quinolinone tested for gastroprotective action and for efficacy to heal experimental gastric ulcers. This drug stimulates prostaglandin generation in gastric mucosa and improves not only the speed but also the quality of ulcer healing. In addition, it protects the gastric mucosa against acute injury caused by various noxious and ulcerogenic factors. Based on these experimental results, rebamipide had been subsequently tested in several clinical trials and approved in Japan for therapeutic use in patients with gastric ulcers and patients with acute gastritis. The main purpose of developing this type of drug was to improve the quality of ulcer healing, especially in that antisecretory drugs lack this advantage. In a preliminary clinical study, rebamipide improved the quality of gastric ulcer healing and reduced future ulcer recurrence. A number of basic research studies have been performed to clarify the mechanisms of rebamipide's action. These studies demonstrated unique properties of rebamipide and convincingly showed that it increases gastric mucus glycoprotein components, stimulates migration and proliferation of wounded epithelial cell monolayers, increases expression of epidermal growth factor and its receptor in normal and ulcerated gastric mucosa, and scavenges active oxygen radicals. The drug also attenuates the activity of neutrophils and the production of inflammatory cytokines stimulated by NSAIDs and/or H. pylori. Therefore, rebamipide can contribute to the management of patients who are taking NSAIDs or are infected with H. pylori. The inhibition of immunoinflammatory responses by rebamipide in H. pylori-infected patients may prevent development of gastritis, peptic ulcer disease, its recurrence, and possibly gastric cancer. Moreover, rebamipide may enhance eradication of H. pylori-infection using standard eradication therapy. Further studies are needed to clarify these possible advantages of rebamipide.
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PMID:Rebamipide: overview of its mechanisms of action and efficacy in mucosal protection and ulcer healing. 975 20


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