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At least 19 recordsLinked to original sources
PubMed1992

[A comparative study of pepsinogen (PG) and lactic acid dehydrogenase (LDH) activities and isoenzyme patterns in tissues from human primary gastric cancer, gastric cancer xenografts in nude mice and gastric cancer cell lines].

Tissue and cell homogenates were prepared for PG and LDH study from 20 samples of histologically proven gastric cancer (GC), 6 samples of gastric cancer xenografts (THPGC-1) of different passages (GCXG) and cultured cells of 3 different gastric cancer cell lines (GCCL). Normal gastric mucosa (NGM) was also obtained from the resected stomach far distant from the primary tumor and histologically tumor free. The results indicated that the expression of PG isoenzymes was low or absent and the PG activities were significantly decreased in GC, GCXG and GCCL as compared to NGM. The activity of LDH was also significantly increased in GC, GCXG and GCCL. In addition, there was a change in isoenzyme pattern in GC and GCXG in which isoenzyme type M was observed whereas isoenzyme type H was preponderent in NGM. The results show that the human gastric cancer xenograft, THPGC-1, has biological properties very similar to those of the primary tumor suggesting that THPGC-1 is a reliable model for the study of the molecular biology of human gastric cancer.

Adenocarcinoma↗
PubMedDate not supplied

[Comparison of the histopathological findings among the biopsies of non-cancerous gastric mucosa of patients with gastric cancer and the biopsies of gastric mucosa of dyspeptic patients without gastric cancer].

Gastric biopsies of the non neoplastic area of 46 patients with gastric cancer and 59 gastric biopsies of dyspeptic patients without gastric cancer were reviewed by one pathologist, without knowing from which group they were coming, to determine the histopathologic findings. The results of both groups were compared. Intestinal metaplasia was found to be significantly higher in gastric cancer patients than in patients without neoplasia (54,3 and 25,4% respectively) (p=0,001). Also in patients with cancer and intestinal metaplasia, this was of the complete type in about 80% of the cases. A number of items were assessed using logistic regression, we found that the presence of complete metaplasia, gastric atrophy and hypertrophy of the mucinogenous vacuole correlates with the presence of gastric cancer (p=0,0159 0,0080 y 0,0280 respectively). H.pylori presence was similar in both groups. The study was done between November 1997 and November 1998 at the Cayetano Heredia National Hospital and the National Institute of Neoplastic Diseases.

Aged↗
PubMed1998

[Differences between Japan and the west in treatment strategy for gastrointestinal cancer--gastric cancer].

Diagnosis, staging, and treatment strategies for gastric cancer were reviewed with regard to differences between Japan and the West. In Japan, detection of early gastric cancer is common due to mass screening and widespread use of endoscopy. Treatment options for gastric cancer vary from endoscopic mucosal resection to the super-extended lymphadenectomy. Correct selection from the available options requires meticulous staging including endoscopy with indigocarmine spray, double contrast barium meal study, endoscopic ultrasonography, CT, abdominal ultrasound, and sometimes barium enema to detect possible peritoneal seeding. Western gastric cancer patients are, on average, 10 years older, more obese, have more cardiopulmonary disease, and more advanced tumors than Japanese patients. Because of the high proportion of patients with extensive disease at presentation in the West, laparoscopic staging is frequently used to avoid non-curative surgery. In Japan, D2 lymphadenectomy is the standard, and now a more extended surgery (D4) is being evaluated in a randomized controlled study, while D2 lymphadenectomy has been reported to be associated with high morbidity and mortality in European studies. Adjuvant chemotherapy is more commonly used in Japan, mostly with oral fluorouracil. However, no regimen has been shown effective in the adjuvant setting in either Japanese and Western studies.

Chemotherapy, Adjuvant↗
PubMed1982

[Clinical and genetic study on human cancer--gastric cancer].

The relationship between gastrointestinal cancers and genetic influence was investigated. The subjects examined were 1211 cancer cases and 781 non-cancer cases registered to the 1st Department of Surgery of Kagoshima University Hospital from 1972 to 1980. The results were as follows: 1. Malignant cases were found in 266/1211 (22.0%) in the families of cancer probandus. Incidence was significantly (P less than 0.01) higher than that [130/781 (16.6%)] in those of non-cancer probandus. 2. Malignant cases were found in 79/356 (22.2%) in the families of gastric cancer probandus and in 51/189 (27.0%) in those of colo-rectal cancer probandus. 3. The relationship between cancer probandus and malignant cases in the families was classified according to the vertical relationship (grandparents-parents-uncle and aunt-probandus-children) and the horizontal relationship (probandus-siblings-cousin). 4. Incidence in the vertical relationships (159/266: 59.8%) was higher than that in the horizontal relationships (107/266: 40.2%). Incidence of the vertical relationships of female cancer probandus (gastric cancer: 70.4%, esophageal cancer: 55.7%, clorectal cancer: 73.9%) was significantly (P less than 0.05) higher than that in those of male cancer probandus. 5. Incidence of blood B type in male gastric cancer group tended to be less when compared with the control group (P less than 0.05). 6. Incidence of smoking habits in esophageal cancer group (82.2%) and the lung cancer group (63.4%) was significantly (P less than 0.01) higher than that in the control group (46.0%). 7. Incidence of drinking habits in the male esophageal cancer group (84.2%) was significantly (P less than 0.01) higher than that in the control group (53.0%).

ABO Blood-Group System↗
PubMed1982

[Distribution of adriamycin in the gastric cancer, gastric wall and regional lymph nodes after a regional arterial infusion].

As a fundamental investigation to prevent from the postoperative recurrence of gastric cancer, the concentrations of adriamycin(ADM) in the gastric tumor, gastric wall and regional nodes were measured after an arterial infusion of 5 or 10 mg of ADM. The drug was infused through either left or right gastric artery or the right gastroepiploic artery at the beginning of operation. The ADM concentration in gastric tumor and gastric wall were moderately elevated after the infusion, especially in the tissue at the area of arterial supply used for the infusion. No significant correlation was found among ADM concentration in the tumor, its histological classification and its amount of interstitial connective tissue. However, the marked elevation of ADM level was confirmed in the perigastric nodes along the drug-infused artery. The moderate elevation was also observed in the 2nd or 3rd group of the regional lymph nodes. As for the drug concentration in the adjacent organs, ADM was detected in slight high level in the liver, less in the spleen and pancreas. From the results obtained, a possibility of prevention from the recurrence of gastric cancer was discussed.

Doxorubicin↗
PubMed1997

Prognostic indicators for cancer. Gastric cancer.

The recent shift in the population from patients presenting with gastric cancer to patients presenting with early-stage lesions has led to renewed interest in identifying prognostic factors for this type of tumor. Conveniently for surgeons, prognostic factors can be divided into groups that are assessed preoperatively, intraoperatively, and postoperatively. Despite the explosion of interest in genetic and molecular markers for gastric cancer, the feature best correlated with patient survival continues to be tumor stage at the time of diagnosis.

Biomarkers, Tumor↗
PubMed1996

Infrequent DPC4 gene mutation in esophageal cancer, gastric cancer and ulcerative colitis-associated neoplasms.

Homozygously Deleted in Pancreatic Cancer 4 (DPC4), a recently identified candidate tumor suppressor gene, was previously shown to be altered in human pancreatic cancers. We examined DPC4 mutation in 30 examples of three other types of gastrointestinal malignancy: 10 esophageal cancers, 10 gastric cancers and 10 colorectal cancers occurring in the preneoplastic condition, ulcerative colitis. The entire coding region of DPC4 (including all 11 exons) was analysed by either direct sequencing of PCR product or the in vitro synthesized protein assay. No coding region mutations of DPC4 were found in any of the samples examined. Our results suggest that inactivation of DPC4 may not be important in the majority of these types of gastrointestinal cancer.

Colitis, Ulcerative↗
PubMed2002

Germline mutations in E-cadherin do not explain association of hereditary prostate cancer, gastric cancer and breast cancer.

Somatic mutations in the E-cadherin (CDH1) gene have frequently been reported in cases with diffuse gastric and lobular breast cancers. Recently, germline mutations have been identified in families with diffuse gastric cancers. In families with hereditary prostate cancer (HPC), a significant association of prostate cancer, gastric and/or breast cancer has been observed in epidemiological studies. The aim of this study was to investigate if germline mutations in CDH1 could explain the risk for cancer in HPC families with an excess of gastric and breast cancer. In total, 17 members from 13 HPC families and 3 members from 3 families with hereditary gastric cancer (HGC) were screened for germline CDH1 sequence alterations using PCR/Denaturing HPLC for initial screening of nucleotide variants followed by confirmatory direct sequencing analysis. The frequency of identified novel germline mutations were tested for in 136 cases with hereditary prostate cancer and 215 cases of sporadic prostate cancer with 422 age matched controls in an allelic discrimination assay. In total, 8 sequence variants were detected in 20 samples tested. In the HPC families, we found 2 missense mutations, A592T in exon 12 and a novel D777N in exon 15 and a mutation in intron 5, 687+92T>A. A previously known polymorphism in exon 13 and 3 sequence variations in introns and untranslated regions were also found, of which the significance is unknown. In HGC-023 with early onset diffuse gastric cancer a truncating mutation, R335X, was identified in exon 7. None of the missense mutations or 687+92T>A were found in the extended HPC material or in the sporadic prostate cancer cases with age-matched controls in the allelic discrimination assay. We found several germline mutations of unknown clinical significance in the CDH1 gene that probably do not explain the association of prostate, gastric and/or breast cancers in the HPC-families. Two missense mutations and a mutation in intron 5 were identified that do not influence the risk of hereditary or sporadic prostate cancer in general and are considered to be pedigree specific. In a family with hereditary gastric cancer of the diffuse type, we identified the first truncating germline mutation in a Scandinavian family.

Adult↗
PubMed1989

[Extended operations in cancer--gastric cancer].

Extended operations of combined resection of surrounding organs and lymphadenectomy of the para-aortic lymph nodes for advanced cancer of the stomach were reported. Combined pancreatoduodenectomy for advanced cancer of lower portion was carried out 5.2% (172/3317). 5 year survival rate was 7% (10/141). Nine 5-year survival cases showed direct invasion to pancreas, so this combined resection is significant for such cases. Left upper abdominal evisceration for advanced cancer of upper and middle portion was carried out in 128 cases (1980-1986). 5-year survival rate was 9.4% (3/32). We expect that this extended procedure shows the progress of surgical results on Borrmann 4 type cancer. Para-aortic lymph node dissection was performed in 400 cases during 10 years (1978-87). The rate of lymph node metastases was 31%. Among them, 5-year survival 5 cases survived over 5 years after operation. For advanced cases with lymph node metastases, lymphadenectomy around the abdominal aorta should be performed more aggressively.

Abdomen↗
PubMed2004

Demethylation of the synuclein gamma gene CpG island in primary gastric cancers and gastric cancer cell lines.

PURPOSE: Whereas synuclein gamma (SNCG) gene expression is usually highly tissue-specific and restricted to the nervous system, SNCG is expressed in advanced-stage breast and ovarian cancers. When overexpressed, SNCG stimulates cancer cell proliferation and metastasis. It is thought that the molecular mechanism of CpG island demethylation may underlie aberrant SNCG expression. To determine whether aberrant SNCG expression and demethylation play a role in gastric carcinogenesis, we examined the expression and methylation status of SNCG in primary gastric cancers, gastric cancer cell lines, and non-neoplastic gastric mucosal tissues. EXPERIMENTAL DESIGN: Ten gastric cancer cell lines, 105 primary gastric cancers, and 10 non-neoplastic gastric mucosal tissues were examined. SNCG expression and methylation status were examined by reverse transcription-PCR and bisulfite-single-strand conformational polymorphism followed by direct sequencing, respectively. The relationship between SNCG methylation status and various clinicopathological factors of the primary gastric cancers was then analyzed. RESULTS: SNCG mRNA expression was observed in 5 of 10 cell lines. Analysis of cell lines positive for SNCG expression revealed that most of the SNCG CpGs were demethylated. SNCG mRNA was not expressed in the 10 non-neoplastic gastric mucosal tissues, although several CpGs were demethylated. Of the 105 primary gastric cancers, 40 (38.1%) showed apparent SNCG demethylation, similar to the result obtained using cell lines. SNCG demethylation was more frequent in primary gastric cancers positive for lymph node metastasis (51%; 26 of 51) than in cancers without lymph node involvement (26%; 14 of 54; P < 0.05), and also more common in stage II-IV (48%; 27 of 56) than in stage I (27%; 13 of 49) cancers (P < 0.05). CONCLUSIONS: Aberrant SNCG gene expression can occur via CpG island demethylation, and tends to occur during the more progressive stages of gastric carcinogenesis.

Adult↗
PubMed2002

Hypermethylation of the TSLC1 gene promoter in primary gastric cancers and gastric cancer cell lines.

The TSLC1 (tumor suppressor in lung cancer-1) gene is a novel tumor suppressor gene on chromosomal region 11q23.2, and is frequently inactivated by concordant promoter hypermethylation and loss of heterozygosity (LOH) in non-small cell lung cancer (NSCLC). Because LOH on 11q has also been observed frequently in other human neoplasms including gastric cancer, we investigated the promoter methylation status of TSLC1 in 10 gastric cancer cell lines and 97 primary gastric cancers, as well as the corresponding non-cancerous gastric tissues, by bisulfite-SSCP analysis followed by direct sequencing. Allelic status of the TSLC1 gene was also investigated in these cell lines and primary gastric cancers. The TSLC1 promoter was methylated in two gastric cancer cell lines, KATO-III and ECC10, and in 15 out of 97 (16%) primary gastric cancers. It was not methylated in non-cancerous gastric tissues, suggesting that this hypermethylation is a cancer-specific alteration. KATO-III and ECC10 cells retained two alleles of TSLC1, both of which showed hypermethylation, associated with complete loss of gene expression. Most of the primary gastric cancers with promoter methylation also retained heterozygosity at the TSLC1 locus on 11q23.2. These data indicate that bi-allelic hypermethylation of the TSLC1 promoter and resulting gene silencing occur in a subset of primary gastric cancers.

Adult↗
PubMed1996

Expression of oncoproteins and the amount of eosinophilic and lymphocytic infiltrates can be used as prognostic factors in gastric cancer. Dutch Gastric Cancer Group (DGCG).

Preoperative staging of gastric cancer is difficult. Several molecular markers associated with initiation and progression of cancer seem promising for obtaining preoperative prognostic information. To investigate whether these markers are indicative especially for the presence of lymph node metastases in patients with gastric cancer, we have examined primary tumour specimens from 105 patients with primary adenocarcinoma of the stomach entered in a surgical trial. In this trial, lymph node status was determined by strictly quality-controlled lymph node dissection and examination. The selected markers were growth regulators (p53, Rb and myc), metastasis-suppressor gene product (nm23), adhesion molecules (Ep-CAM, E-cadherin, CD44v5 and CD44v6) and urokinase-type plasminogen activator (u-PA). Also, the amount of eosinophilic and lymphocytic infiltrates available post-operatively was analysed with respect to its prognostic value for lymph node status. Moreover, the association of these parameters with survival and disease-free period (DFP) was evaluated. Of all molecular markers investigated, only Rb expression had a significant association with the presence of lymph node metastasis in both univariate and multivariate analysis. For curative resectability, a significant association was found with Rb and E-cadherin expression, while in multivariate analysis Rb and myc were selected as the combination with additional independent prognostic value, and E-cadherin had no additional independent value. For overall survival in univariate analysis, the amount of both eosinophilic and lymphocytic infiltrates and Rb and myc expression were of significant prognostic value. Only the amount of lymphocytic infiltrate had a prognostic significance for DFP. In stepwise multivariate analysis, TNM stage (I + II) and marked lymphocytic infiltrate were associated with better overall survival and longer DFP. We conclude that, if these results are confirmed in a larger series of patients, molecular markers can provide useful prognostic information.

Aged↗
PubMed2002

Molecular biology of gastric cancer.

Gastric cancer is one of the leading causes of cancer mortality in the world. Gastric adenocarcinomas account for more than 95% of gastric tumors, whereas gastrointestinal stromal tumors (GISTs) are the most common neoplasms of the rare gastric mesenchymal tumors. Although the incidence of mid-distal gastric adenocarcinomas is decreasing, the incidence of gastroesophageal junctional tumors and Barrett's adenocarcinomas is increasing for unknown reasons. The majority of gastric tumors are sporadic in nature. However, there are rare, inherited gastric cancer predisposition traits, such as germline p53 (Li-Fraumeni syndrome) as well as E-cadherin (CDH1) alterations in familial diffuse gastric cancers. Gastric cancer has been observed to be part of the spectrum of neoplasms associated with germline mismatch repair gene (MMR) alterations that give rise to the hereditary nonpolyposis colorectal cancer (HNPCC) entity. Comparative genomic hybridization analyses have identified several amplifications and losses of DNA copy numbers in gastric cancers. Loss of heterozygosity (LOH) studies have shown several chromosomal loci with significant allelic loss, thus indicating the possibility of harboring a tumor suppressor gene important in gastric tumorigenesis. Microsatellite instability (MIS) and associated alteration of the TGF-bIIR, IGFRII, BAX, E2F-4, hMSH3, and hMSH6 genes are found in a subset of gastric carcinomas. Cell adhesion molecule abnormalities such as those involving CDH1 may play an important role in diffuse-type gastric cancer development. Although, multiple somatic alterations have been described in gastric carcinomas at the molecular level, the significance of these changes in gastric tumorigenesis remains to be established in most instances. The critical molecular alterations in gastric cancers that may lead to advances in our armamentarium to combat this lethal disease remain to be fully characterized.

Adenocarcinoma↗
PubMed1994

Helicobacter pylori: the link with gastric cancer.

Gastric cancer is the world's overall second most common cancer, and carries a bad prognosis. In the Correa model of gastric carcinogenesis, environmental factors (salt, nitrate, a lack of vitamin C and beta-carotene, bile reflux, bacterial overgrowth in atrophic gastritis with nitrosamine formation) are related to the evolution from normal gastric tissue through superficial gastritis, multifocal atrophic gastritis, intestinal metaplasia and dysplasia to carcinoma. The incidence of H. pylori decreases with progressing preneoplastic lesions. In several studies, the prevalence of H. pylori was elevated in patients with gastric cancer, with a trend for a higher prevalence in intestinal type gastric cancer vs diffuse type. Family members of patients with gastric adenocarcinoma have a higher H. pylori prevalence than controls; patients infected with H. pylori have more family members with gastric cancer. Several epidemiological studies showed a higher H. pylori prevalence in regions or populations with high gastric cancer risk vs low-risk populations. Large-scale studies in China and Europe showed a correlation between H. pylori seroprevalence and gastric cancer incidence and mortality. Three prospective nested case-control studies showed that infection with H. pylori increased the risk of further development of gastric adenocarcinoma, showing that H. pylori infection precedes the development of gastric cancer. Several pathways can be identified explaining the association between H. pylori and gastric adenocarcinoma. We showed that gastric cell proliferation is increased in parallel with inflammation. The ascorbic acid concentrating mechanism is abolished in gastritis. Ammonia, generated by H. pylori's urease, gives rise to gastric mucosal atrophy. We showed that salt increases the gastric cell proliferation only in H. pylori-infected individuals. The organism's toxin may play a role in gastric cancer. Besides H. pylori, other environmental factors are important in determining the gastric cancer risk. For instance, we showed that in Belgium, Maghreb immigrants have a high prevalence of H. pylori infection but a low prevalence of intestinal metaplasia and gastric cancer. Gastric lymphoma is rare (about 5% of all gastric tumours), but its incidence is steadily increasing. It was shown that H. pylori also increases the risk for low-grade as well as high-grade gastric lymphoma. Eradication of H. pylori has been shown to cure several cases of unequivocally proven gastric low-grade lymphoma.(ABSTRACT TRUNCATED AT 400 WORDS)

Helicobacter Infections↗