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)

Elevated levels of the calcium-binding protein S100A4 cause metastasis of benign rat mammary tumor cells. To investigate whether S100A4 plays an important role in the invasion and metastasis of gastric cancers, we examined the gene mutations in the coding regions and expression patterns of the S100A4 in gastric adenocarcinoma in Korea. Moderate to strong expression of S100A4 was found in 53 (68.8%) of the 77 gastric adenocarcinomas, whilst normal gastric epithelium either failed to stain or showed weak staining. Interestingly, S100A4 expression was more frequently observed in gastric cancer patients with advanced gastric cancer (p=0.039), positive lymph node metastasis (p=0.001), and peritoneal dissemination (p=0.022). No gene mutations were found in the analyzed genomic area in 77 gastric adenocarcinomas and 15 gastric cancer cell lines. We found one single nucleotide polymorphism without an amino acid change, A99G, in two cases. These data suggest that the overexpression of S100A4 may be closely related to the aggressiveness of gastric cancer in Korea.
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PMID:Overexpression of S100A4 is closely related to the aggressiveness of gastric cancer. 1288 5

Positron emission tomography (PET) with (18)F-2-deoxy-2-fluoro-D-glucose (FDG) has been investigated as a means of detecting certain primary tumors and their metastatic disease in recent years. The aim of this study was to compare the performance of FDG-PET and operative assessment with formal pathologic staging. Altogether, 85 patients had undergone surgical treatment for gastric cancer with curative intent, with FDG-PET preoperatively. The results using FDG-PET were compared with those using computed tomography (CT); they were also correlated with the pathologic findings. For quantitative analysis, the regional tumor uptake was measured by the standard uptake value (SUV) using a region of interest technique. Using FDG-PET, the primary tumor was visualized in 75.2% of patients. A comparison of the FDG uptake and the clinicopathologic findings showed that there was a significant association between FDG uptake and the depth of invasion, the size of the tumor, and lymph node metastasis. FDG-PET scans had less accuracy for diagnosing locoregional lymph nodes than CT because of a significant lack of sensitivity (23.3% vs. 65.0%). The survival rate for patients with high FDG uptake (SUV > 4) was significantly lower than that for those with low FDG uptake (SUV < 4) ( p < 0.05). FDG-PET was successful in detecting the primary gastric cancer lesion but not for finding early-stage gastric cancers. Detection of nodal metastasis also was not possible by FDG-PET. However, FDG-PET appears to provide important additional information concerning the aggressiveness of the tumor and the prognosis in patients with gastric cancer.
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PMID:Evaluation of 18F-2-deoxy-2-fluoro-D-glucose positron emission tomography for gastric cancer. 1496 Nov 97

Gastric cancer is the second most common cause of cancer-related death worldwide and the highest incidence of this cancer has been reported in Asia, especially in China. Identification of early stage lesions is vital in achieving high survival rate. However, due to the lack of reliable biomarkers, the majority of gastric cancer is presented at an advanced stage. Recently, it has been reported that Id-1, a helix-loop-helix protein, may be a valuable diagnostic marker in many types of human cancer. In this study, we evaluated Id-1 protein expression in gastric cancer specimens and compared it with non-malignant tissues. In addition, to investigate whether Id-1 expression levels were associated with the aggressiveness of this disease as implicated in other cancer types, we also assessed Id-1 expression levels in primary tumours and their lymph node metastasized lesions. Our results indicate that up-regulation of Id-1 is a frequent event in gastric cancer but its expression levels are not associated with tumour metastasis. Our evidence provides a possible novel marker for the diagnosis of gastric cancer.
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PMID:Overexpression of Id-1 in gastric adenocarcinoma: implication for a novel diagnostic marker. 1516 Oct 41

Due to the contradictory roles that thymidine phosphorylase (TP) plays in both tumor aggressiveness and fluoropyrimidine activation, its impact on drug responses has yet to be clearly established. Therefore, the present study was performed to clarify the effects of TP levels on the prognosis of gastric cancer patients treated postoperatively with different fluoropyrimidines. A total of 52 gastric cancer patients who underwent gastrectomy from January 1997 to March 1998 were enrolled in the present study. The TP levels in the specimens were assayed by enzyme-linked immunosorbent assay (ELISA). Survival was significantly poorer for the 27 patients with high normal tissue TP activity than for the 25 with low normal tissue TP activity. Normal tissue TP level showed different effects on survival according to the chemotherapy regimen used. While the survival rate was significantly poorer in patients with high normal TP level than in those with low normal TP in the 5-FU group, the rate was almost the same in the 5'-DFUR group. Cox's proportional hazard model revealed that tumor TP was an independent prognostic factor in gastric cancer patients. Since activating and catabolizing enzymes for fluoropyrimidines differ from each other, alterations in gene expression of these enzymes should be useful predictive factors.
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PMID:Effects of thymidine phosphorylase levels in cancer, background mucosa, and regional lymph nodes on survival of advanced gastric cancer patients receiving postoperative fluoropyrimidine therapy. 1554 51

Accumulated evidence has established that aberrant regulation of histone deacetylases (HDACs) is one of the major causes of the development of human malignancies. Among different iso-enzymes of HDAC and sirtuins grouped as the HDAC super family, little is known as to how histone deacetylase 2 (HDAC2) causes carcinogenesis in solid tumors. Here, in order to investigate the possible role of HDAC2 in gastric carcinogenesis, we analyzed the expression of HDAC2 in 71 gastric adenocarcinomas by immunohistochemistry. Moderate to strong expression of HDAC2 was found in 44 (62%) out of a total of 71 tumors. The majority of positive tumors, which were detected in the nucleus but not in normal gastric epithelium, did not express HDAC2 or showed only weak positive staining. Interestingly, we also noted that HDAC2 expression appeared to be associated with tumor aggressiveness as HDAC2 expression was observed to be statistically significant in advanced gastric cancer (P=0.0023, Chi-square test) and in positive lymph node metastasis (P=0.0713, Chi-square test). Taken together, these results suggest that HDAC2 may play an important role in the aggressiveness of gastric cancer.
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PMID:Increased expression of histone deacetylase 2 is found in human gastric cancer. 1586 7

Wnt-5a is a representative ligand that activates a beta-catenin-independent pathway in the Wnt signaling. Although abnormal activation of beta-catenin-dependent pathway is often observed in human cancer, the relationship between beta-catenin-independent pathway and tumorigenesis is not clear. We sought to clarify how Wnt-5a is involved in aggressiveness of gastric cancer. Abnormal expression of Wnt-5a was observed in 71 of 237 gastric cancer cases by means of immunohistochemistry. The positivity of Wnt-5a expression was correlated with advanced stages and poor prognosis of gastric cancer. Wnt-5a had the abilities to stimulate cell migration and invasion in gastric cancer cells. Wnt-5a activated focal adhesion kinase and small GTP-binding protein Rac, both of which are known to play a role in cell migration. Cell migration, membrane ruffling, and turnover of paxillin were suppressed in Wnt-5a knockdown cells. Furthermore, anti-Wnt-5a antibody suppressed gastric cancer cell migration. These results suggest that Wnt-5a stimulates cell migration by regulating focal adhesion complexes and that Wnt-5a is not only a prognostic factor but also a good therapeutic target for gastric cancer.
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PMID:Expression of Wnt-5a is correlated with aggressiveness of gastric cancer by stimulating cell migration and invasion. 1707 65

The human homolog of the Drosophila prune protein (from PRUNE, which encodes h-prune), which interacts with glycogen synthase kinase 3, promotes cellular motility. H-prune also interacts with nm23-H1, a suppressor of cancer metastasis. It has been reported that stimulation of cellular motility by h-prune is enhanced by its interaction with nm23-H1 in breast cancer cells. In the present study, we examined the expression of h-prune and nm23-H1 during tumor progression in gastric cancer (GC). PRUNE mRNA was overexpressed in 12 (32%) of 38 GC cases by quantitative reverse transcription-polymerase chain reaction. PRUNE mRNA levels correlated significantly with advanced T grade, N grade and tumor stage. Immunohistochemical analysis revealed that 43 (30%) of 143 GC cases were positive for h-prune, and h-prune-positive GC cases showed more advanced T grade, N grade and tumor stage than h-prune-negative GC cases. One hundred and twenty-four (87%) of 143 GC cases were positive for nm23-H1, and nm23-H1 was expressed in almost all (42 cases, 98%) h-prune-positive GC cases. Many GC cases positive for both h-prune and nm23-H1 showed more advanced T grade, N grade and tumor stage than other type GC cases. Patients with h-prune-positive GC had a significantly worse survival rate than patients with h-prune-negative GC. These findings indicate that overexpression of h-prune is associated with tumor progression and aggressiveness of GC. nm23-H1 may enhance motility of cancer cells by interacting with h-prune.
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PMID:Increased expression of h-prune is associated with tumor progression and poor survival in gastric cancer. 1753 57

Angiopoietin-2 (Ang-2) and vascular endothelial growth factor (VEGF) contribute to gastric cancer aggressiveness by up-regulating the expression of proteases. We evaluated the expression and the prognostic significance of angiogenic factors and proteases in 148 patients with R0-resected gastric cancer. Expression of VEGF, Ang-2, cyclooxygenase-2 (COX-2), urokinase-type plasminogen activator (uPA) and its inhibitor PAI-1, matrix metalloproteinases (MMP)-1 and -9 were assayed by immunohistochemistry. After a mean of 63 +/- 4 months, 81 out of 148 patients had died due to disease. The probability of being free of recurrence was 62, 48, and 42% at 2, 5, and 10 years, respectively. Single bivariate analysis identified VEGF, Ang-2, COX-2, PAI-1, and MMP-9 expression, along with several clinicopathological parameters (grade of curability, lymph node ratio, pTNM, pT, pN), as variables associated with both decreased disease-specific survival and recurrence. On multivariate analysis, after adjusting for significant clinical covariables, positive VEGF immunostaining was the primary prognostic factor, and no other tumor marker variable could add any significant improvement for the prediction, for both disease-specific survival (p = 0.001; HR, 3.27; 95% CI, 1.76 to 6.10) and tumor recurrence (p = 0.002; HR, 2.81; 95% CI, 1.48 to 5.35). Our study suggests that VEGF alone may be clinically useful for establishing therapeutic decisions in gastric cancer patients.
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PMID:Positive VEGF immunostaining independently predicts poor prognosis in curatively resected gastric cancer patients: results of a study assessing a panel of angiogenic markers. 1797 43

Gastric cancer is one of the most common cancers and the second most common cause of cancer deaths worldwide. Apart from Japan, where screening programmes have resulted in early diagnosis in asymptomatic patients, in most countries the diagnosis of gastric cancers is invariably made on account on dyspeptic and alarm symptoms, which may also be of prognostic significance when reported by the patient at diagnosis. However, their use as selection criteria for endoscopy seems to be inconsistent since alarm symptoms are not sufficiently sensitive to detect malignancies. In fact, the overall prevalence of these symptoms in dyspeptic patients is high, while the prevalence of gastro-intestinal cancer is very low. Moreover, symptoms of early stage cancer may be indistinguishable from those of benign dyspepsia, while the presence of alarm symptoms may imply an advanced and often inoperable disease. The features of dyspeptic and alarm symptoms may reflect the pathology of the tumour and be of prognostic value in suggesting site, stage and aggressiveness of cancer. Alarm symptoms in gastric cancer are independently related to survival and an increased number, as well as specific alarm symptoms, are closely correlated to the risk of death. Dysphagia, weight loss and a palpable abdominal mass appear to be major independent prognostic factors in gastric cancer, while gastro-intestinal bleeding, vomiting and also duration of symptoms, do not seem to have a relevant prognostic impact on survival in gastric cancer.
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PMID:Role of symptoms in diagnosis and outcome of gastric cancer. 1830 Mar 38

Gastric cancer is of major importance world-wide being the second most common cause of cancer-related death in the world. According to Lauren's histological classification gastric cancer is divided in two groups, the better differentiated intestinal carcinomas and the poorly differentiated diffuse-type cancers. The genetic changes underlying the initiation and progression of gastric cancer are not well defined. Gastric carcinogenesis is a multistep process involving a number of genetic and epigenetic factors. Although it has been proposed that different genetic pathways exist for differentiated and undifferentiated carcinomas, the two histological subtypes of gastric cancer share some common genetic alterations. Currently, tumor histology and pathologic stage are the major prognostic variables used in the clinical practice for gastric cancer patients. However, it is known that tumors with similar morphology may differ in biological aggressiveness, prognosis and response to treatment. Molecular genetic analysis of gastric cancer revealed a number of associations of certain genetic changes with pathological features, tumor biological behavior and prognosis of gastric cancer patients, suggesting that these genetic abnormalities might play an important role in gastric tumorigenesis. Increasing evidence suggests that the molecular genetic changes could be helpful in the clinical setting, contributing to prognosis and management of patients. Regarding epigenetic events in gastric tumorigenesis, a number of methylating markers have been proposed for risk assessment, prognostic evaluation and as therapeutic targets. However, further research is required in order to systematically investigate the genetic changes in gastric cancer estimating also their usefulness in the clinical practice. A good understanding of the genetic changes underlying gastric carcinogenesis may provide new perspectives for prognosis and screening of high risk individuals. Some of the genetic alterations could definitely improve tumor classification and management of gastric cancer patients. Also, based on molecular data identified in gastric cancer novel therapeutics might help to improve the treatment of this disease.
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PMID:Cytogenetic and molecular aspects of gastric cancer: clinical implications. 1838 Dec 31


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