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)

The influence of standard lymphadenectomy on the occurrence of damage to the pancreas was evaluated in 28 patients with gastric cancer, by analysing related serum and urine enzyme activities, pre- and postoperatively. Enzymatic evidence for pancreatic damage was related to the surgical procedure performed. Postoperatively, the patients treated by R2 gastrectomy had significantly increased levels of P-type amylase in the serum compared with findings in patients treated by R1 gastrectomy or bypass procedures. Conversely, the S-type amylase in both groups remained within normal limits during the study period. Pancreatic secretary trypsin inhibitor (PSTI) and phospholipase A2 (PLA2) proved to be less sensitive to pancreas damage caused by lymphadenectomy. The R2 patients with P-type hyperamylasemia had no major postoperative complications. Thus, while the standard R2 gastrectomy may well be a relevant factor associated with the occurrence of transient P-type hyperamylasemia, there seems to be no relation to major postoperative complications such as pancreatitis.
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PMID:Hyperamylasemia associated with lymphadenectomy in patients surgically treated for gastric cancer. 137 23

To investigate the role of group II phospholipase A2(PLA2) in cancer, we examined the expression and secretion of group II PLA2 in response to the stimulation of interleukin 6(IL-6) in human gastric cancer cells in vitro. Group II PLA2 determined by a specific radioimmunoassay was constitutively produced in culture supernatant of KATO III (signet ring cell carcinoma) and MKN28 (well differentiated adenocarcinoma). This production in KATO III significantly increased with a treatment of IL-6, whereas that in MKN28 remained at a same level. Moreover, the quantitation by reverse transcription-polymerase chain reaction(RT-PCR) demonstrated the IL-6 inducible overexpression of group II PLA2 mRNA in KATO III. This transcription was mediated by NF-IL6, the same as in hepatocytes. These results suggest two possible mechanisms of group II PLA2 production by cancer cells in vivo, that is, cytokine-induced production and constitutive production.
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PMID:Group II phospholipase A2 in invasive gastric cancer cell line is induced by interleukin 6. 811 91

The expression of Group-II phospholipase A2 (M-PLA2) was analysed immunohistochemically in malignant, non-malignant (including atrophic, hyperplastic, pseudopyloric metaplastic and intestinal metaplastic) and normal human gastric mucosae. M-PLA2 was consistently detected in the stem cell lineage, pseudopyloric metaplasia and the generative cells of hyperplastic foveolar epithelium and intestinal metaplasia (IM). In IM, the appearance of M-PLA2 was found to be closely related to the degree of development of the brush borders on columnar cells and was especially prominent at dense brush borders. Paneth cells of IM, particularly their secretory products, were strongly immunoreactive for M-PLA2. In gastric cancer, the expression of M-PLA2 was detected exclusively in cancer cells with a low grade of differentiation, and seemed to be intensified in the invading zone of the tumour. These observations suggest that the expression of M-PLA2 is associated with the proliferative kinetics and regeneration of human gastric mucosa, and may indicate a physiological relationship between its expression and metaplasia of small intestinal type. Moreover, the appearance of M-PLA2 may be related to the invasive ability of gastric cancer.
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PMID:Expression of group-II phospholipase A2 in malignant and non-malignant human gastric mucosa. 831 99

Helicobacter pylori infection has been linked to the development of gastritis which can then progress to a number of disease entities including peptic ulcer disease and gastric cancer. Since the pathogenic mechanism by which the bacteria causes gastritis is unresolved, we employed a model system, the H. felis-infected mouse to investigate the temporal relationship between bacterially-induced alterations in the hydrophobic phospholipid barrier of the stomach and the development of gastritis. In the present study, C57BL/6 mice were inoculated with 10(9) CFU of H. felis and the changes in gastric wet weight, histology, surface hydrophobicity, phospholipid/phosphatidylcholine concentration, phospholipase A2 activity, and the pH of collected gastric juice were measured 0.5-2 months postinoculation. In related experiments, we investigated the effects of treating H. felis infected mice with antibiotic/ bismuth therapy on the above gastric properties. It was determined that both gastric surface hydrophobicity and phospholipid composition were significantly attenuated as early as 2-4 weeks postinfection, preceding signs of mucosal inflammation and glandular atrophy as indicated by increases in gastric wet weight, pH and a disappearance in parietal cells. These early H. felis-induced changes in gastric surface hydrophobicity and phospholipid concentration were reversed by antibiotic/bismuth therapy. Based on these results we conclude that H. felis infection induces an early transformation of the stomach from a hydrophobic to an acid-sensitive hydrophilic state that may trigger the subsequent development of gastritis.
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PMID:Attenuation of hydrophobic phospholipid barrier is an early event in Helicobacter felis-induced gastritis in mice. 995 31

The high incidence of biliary tract carcinoma in patients with anomalous pancreaticobiliary ductal junction (APBDJ) has been well documented. Elevation of the secondary and free bile acid (FBA) concentrations is considered a risk factor for biliary carcinogenesis in these patients. Bile from the gallbladder and common bile duct in 12 patients with APBDJ was analyzed and compared with gallbladder bile from 19 patients with gastric cancer and a normal hepatobiliary tract. The concentrations of secondary bile acids were significantly lower in the APBDJ group than in the control group, and FBA concentrations were not detected in the gallbladder in either group. The lysolecithin (LL) in the phospholipid, which is produced from lecithin by activated phospholipase A(2) in refluxing pancreatic juice, was significantly elevated in the APBDJ group. Elevation of the LL concentration in the bile is one of the factors for the development of biliary tract carcinoma in patients with APBDJ.
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PMID:Altered bile composition in the gallbladder and common bile duct of patients with anomalous pancreaticobiliary ductal junction. 1059 97

BACKGROUND: In Japan, much attention has recently been paid to super-extended paraaortic lymphadenectomy (PAL) for the treatment of advanced gastric cancer. However, it has been reported that PAL is associated with increased morbidity and mortality, as compared to conventional extended lymphadenectomy (D2 or D3). Therefore, an analysis of the effects of PAL on perioperative changes in the biological responses of patients essential for determining the potential utility of this procedure.METHODS: The current non-randomized prospective study included evaluations of perioperative changes in parameters of surgical stress (series I; serum levels of antidiuretic hormone, interleukin-6, trypsin, and phospholipase A(2)) and immunocompetence (series II; phytohemagglutinin- and concanavalin A-induced blastogenesis, activity of natural killer cells and the ratio of CD4 cells to CD8 cells) in patients with advanced gastric cancer (T3 or T4), comparing groups treated with D3 plus PAL ( n = 12) and D3 ( n = 13), and a control group with early gastric cancer ( n = 16) treated with D1 lymphadenectomy (perigastric N1 nodes) between April 1995 and April 1997.RESULTS: The duration of surgery and the amount of blood lost were longer and greater in the D3 plus PAL group than in the D3 and D1 groups. D3 plus PAL and D3 were associated with significant postoperative increases in parameters of surgical stress, as well as with significant postoperative immunosuppression, compared to results with D1. However, there were no significant differences in the respective parameters between the D3 plus PAL and D3 groups.CONCLUSIONS: Our results indicate that there are no essential differences in patients' biological responses between D3 plus PAL and D3 lymphadenectomy. It appears that PAL-associated morbidity can be minimized by very careful manipulation during the dissection of paraaortic lymph nodes.
Gastric Cancer 1998 Dec
PMID:Effects of super-extended paraaortic lymphadenectomy (PAL) on biological responses in totally gastrectomized patients with T3 or T4 gastric cancer. 1195 44

Phospholipase D (PLD) catalyzes the hydrolysis of phosphatidylcholine to generate phosphatidic acid (PA) and choline. There are at least two PLD isozymes, PLD1 and PLD2. Genetic and pharmacological approaches implicate both PLD isozymes in a diverse range of cellular processes, including receptor signaling, membrane transport control, and actin cytoskeleton reorganization. Several recent studies reported that PLD has a role in signaling pathways that oppose apoptosis and promote cell survival in cancer. In this study, we examined the role of PLD in taxotere-induced apoptosis in stomach cell lines; normal stomach (NSC) and stomach cancer cells (SNU 484). Taxotere treatment resulted in increase of PLD activity. To confirm the role of PLD in taxotere-induced apoptosis, PLDs were transfected into SNU 484 cells. Overexpression of PLD isozymes resulted in inhibition of taxotere-induced apoptotic cell death, evidenced by decreased degradation of chromosomal DNA, and increased cell viability. Concurrently, Bcl-2 expression was upregulated, and taxotere-induced activation of procaspase 3 was inhibited after PLD's transfection. However, when PLD was selectively inhibited by specific siRNA-PLD1 or -PLD2, taxotere-induced apoptosis was exacerbated in SNU 484 cells. On top of this, PA -- the product of PLDs, also resulted in upregulation of Bcl-2 in SNU 484. Although PA-induced Bcl-2 expression was blocked by mepacrine, an inhibitor of phospholipase A(2) (PLA(2)), increased Bcl-2 expression by PA was not abrogated by propranolol, an inhibitor of PA phospholyhydrolase (PAP). Taken together, PLD1 and PLD2 are closely related with Bcl-2 expression together with PLA(2), but not with PAP, during taxotere-induced apoptosis in SNU 484 cells.
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PMID:Overexpression of phospholipase D suppresses taxotere-induced cell death in stomach cancer cells. 1819 Jul 95

We examined the immunohistochemical expression of membrane-associated phospholipase A(2) (M-PLA(2)), belonging to group II PLA(2), in 44 advanced gastric cancers, using the ABC method and monoclonal antibody anti-human M-PLA(2). M-PLA(2) mRNA was also examined in the same rumours by Northern blot analysis. In addition, the content of M-PLA(2) protein and prostaglandin E(2) (PGE(2)) in the malignant lesion and in the non-malignant gastric mucosa was examined. The expression was detected in cancer cells in 31 out of 44 advanced gastric cancer tissues (70.4%) by the ABC method. M-PLA(2) mRNA was detected in 36 out of 44 gastric cancer tissues (81.8%), and the density was observed to be higher in tumour tissues than in the adjacent nonmalignant gastric mucosa. The M-PLA(2) protein was detected both in malignant tissues and in non-malignant gastric mucosa, and the content of M-PLA(2) protein was significantly higher in malignant tissues than in the non-malignant gastric mucosa. There was a significant positive correlation between the expression of M-PLA(2) mRNA and the amount of M-PLA(2) protein. PGE, was also detected in the malignant tissues and in the non-malignant mucosa. The content of PGE, was significantly higher in the former. These results indicate that M-PLA(2) is produced both in malignant and nonmalignant cells of the stomach, the former producing higher amounts of this enzyme than the latter. M-PLA(2) may be involved in cancer progression through its function or through the function of products of this enzyme's action such as PGE(2) in gastric cancer.
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PMID:Production of group II phospholipase A(2) in advanced gastric cancer. 2154 43

Arachidonic acid metabolic pathway has been implicated in the inflammation-associated tumorigenesis of gastrointestinal cancers. As the rate-limiting enzyme of arachidonic acid production, group IVA phospholipase A2 (PLA2G4A) is hypothesized to play a fundamental role in gastric tumorigenesis as well as cyclooxygenase-2 (COX-2). However, little is known about the expression and role of PLA2G4A in gastric cancer, and the association of PLA2G4A with COX-2 remains to be elucidated. In this study, the mRNA expression of PLA2G4A and COX-2 in 60 pairs of fresh gastric tumors and corresponding adjacent non-cancerous mucosa was detected by using real-time quantitative PCR and the immunostaining of the both proteins in paired samples from 866 gastric cancer patients were assessed by using immunohistochemistry method. The clinicopathological and the prognostic relevance of PLA2G4A and COX-2 expression were determined. The results revealed a significantly reduced expression of PLA2G4A in gastric tumors compared to in non-cancerous tissues, as opposite to the increased expression of COX-2. PLA2G4A was significantly associated with tumor size (P = 0.003), tumor grade (P < 0.001), intestinal type (P = 0.003), T classification (P < 0.001), N classification (P < 0.001), and thereby TNM stage (P < 0.001). PLA2G4A and COX-2 expression were both identified as independent prognostic factors in multivariate Cox model analysis (P = 0.024 for PLA2G4A and P < 0.001 for COX-2). Moreover, the reduced PLA2G4A and increased COX-2 expression was both associated with unfavorable survival for patients with gastric cancer. PLA2G4A might serve as a promising target for future therapeutic approaches to gastric cancer combined with COX-2 inhibitors.
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PMID:Reduced group IVA phospholipase A2 expression is associated with unfavorable outcome for patients with gastric cancer. 2330 60

Growing evidence suggests that phospholipase A2 (PLA2) plays a pivotal role in tumorigenesis in human gastrointestinal cancer. One of the well-studied isoforms of PLA2, group IIA PLA2 (PLA2G2A), appears to exert its protumorigenic or antitumorigenic effects in a tissue-specific manner. The present study was designed to determine the expression profile and prognostic value of PLA2G2A in gastric cancer in a large Chinese cohort. By using real-time polymerase chain reaction, the amount of PLA2G2A messenger RNA in 60 pairs of fresh gastric tumors and adjacent noncancerous mucosa was measured. The immunostaining of PLA2G2A in 866 gastric cancers with paired noncancerous tissues was assayed. No expression of PLA2G2A was found in normal gastric mucosa, and focal expression of PLA2G2A was noticed in intestinal metaplasia, whereas significantly increased expression of PLA2G2A was observed in the cytoplasm of gastric cancer cells. Furthermore, the extent of PLA2G2A expression was associated with tumor size (P < .001), tumor differentiation (P = .001), T class (P < .001), N class (P < .001), and TNM stage (P < .001) of gastric cancer. Multivariate analysis showed that PLA2G2A expression was an independent predictor of survival for patients with gastric cancer (P = .024). Expression of PLA2G2A seems to be protective for patients with gastric cancer (hazard ratio, 1.423; 95% confidence interval, 1.047-1.935), and it may be a target for achieving better treatment outcomes.
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PMID:Expression of group IIA phospholipase A2 is an independent predictor of favorable outcome for patients with gastric cancer. 2366 39


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