• Journal of Gastric Cancer
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• v.1 no.4
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• pp.202-209
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• 2001

Purpose: When cancer cels invade the stroma, they should be dissociated from the adjacent cells at first. E-cadherin and $\beta-catenin$ constitute an important protein complex associated with cellular adhesion, development, and differentiation, especially in epithelial cells. The role of E-cadherin and $\beta-catenin$ in gastric carcinogenesis were studied. Materials and Methods: The expression of E-cadherin and $\beta-catenin$ in gastric adenocarcinomas by using immunohistochemical staining and the mutation by using polymerase chain reaction- single stranded conformation polymorphism (PCR-SSCP) and sequencing were performed in 40 adenocarcinomas and 5 dysplasia of stomach. Thirteen cases, which had lymph node metastasis, were also included for immunohistochemical staining. Results: Inappropriate cytoplasmic and/or nuclear expression of a E-cadherin-$\beta-catenin$ complex was more frequent in poorly differentiated, diffuse type signet ring cell carcinomas than in well-differentiated, intestinal type adenocarcinomas (P<0.05). However, the expression was not related with clinical stage or lymph node metastasis. Mutation of E-cadherin was detected in 4 cases by using PCR-SSCP, whereas mutation of $\beta-catenin$ was detected in 2 cases. Conclusion: E-cadherin and $\beta-catenin$ seem to be important in gastric carcinogenesis, especially in poorly differentiated diffuse type.

• Journal of Gastric Cancer
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• v.17 no.1
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• pp.63-73
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• 2017

Purpose: Data on operable gastric cancer from India is sparse. The purpose of this study was to investigate the clinical details, histopathological demographics, and 5-year overall survival (OS) and disease free survival (DFS) associated with operable, non-metastatic gastric cancer in a dedicated upper gastrointestinal (GI) surgical unit in India. Materials and Methods: Data for patients diagnosed with operable gastric cancer between January 2006 and December 2014 were retrospectively analyzed. Data were collected from electronic hospital records in addition to mail and telephonic interviews when possible. Results: A total of 427 patients were included. The tumor was located in the pyloro-antral region in 263 patients (61.7%). Subtotal gastrectomy was performed in 291 patients and total gastrectomy in 136 patients. Tumor stage classification revealed 43 patients (10.0%) with stage I, 40 patients (9.4%) with stage IIA, 59 patients (13.9%) with stage IIB, 76 patients (17.8%) with stage IIIA, 96 patients (22.5%) with stage IIIB, and 113 patients (26.4%) with stage IIIC disease. Follow-up data were available for 71.6% of the patients with a mean duration of 32.4 months. Five-year DFS and OS were 39% and 59%, respectively. Conclusions: Despite presenting at an advanced stage, the 5-year DFS and OS of patients with operable gastric cancer treated at a dedicated upper GI unit of a tertiary care center in India was good.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.4
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• pp.1377-1382
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• 2012

Morphine is not only an analgesic treating pain for patients with cancer but also a potential anticancer drug inhibiting tumor growth and proliferation. To gain better insight into the involvement of morphine in the biological characteristics of gastric cancer, we investigated effects on progression of gastric carcinoma cells and the expression of some apoptosis-related genes including caspase-9, caspase-3, survivin and NF-${\kappa}B$ using the MGC-803 human gastric cancer cell line. The viability of cells was assessed by MTT assay, proliferation by colony formation assay, cell cycle progression and apoptosis by flow cytometry and ultrastructural alteration by transmission electron microscopy. The influences of morphine on caspase-9, caspase-3, survivin and NF-${\kappa}B$ were evaluated by semi-quantitative RT-PCR and Western blot. Our data showed that morphine could significantly inhibit cell growth and proliferation and cause cell cycle arrest in the G2/M phase. MGC-803 cells which were incubated with morphine also had a higher apoptotic rate than control cells. Morphine also led to morphological changes of gastric cancer cells. The mechanism of morphine inhibiting gastric cancer progression in vitro might be associated with activation of caspase-9 and caspase-3 and inhibition of survivin and NF-${\kappa}B$.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.10
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• pp.5735-5740
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• 2013

Background: A number of studies have investigated the association between increased pretreatment serum C-reactive protein (CRP) levels and the prognosis of gastric cancer. However, due to the inconsistent results, whether the serum CRP level can be a prognostic factor in primary gastric cancer remains controversial. Methods: We searched Medline, PubMed, Embase and the Cochrane Central Register of Controlled Trials for relevant high-quality reports. A meta-analysis was carried out using the included studies to assess the association between pretreatment serum CRP level and overall survival (OS) in patients with gastric cancer. Correlation analyses were conducted to evaluate the relationship between serum CRP and tumor characteristics such as tumor node metastasis (TNM) stage and recurrence. Results: Twelve reports involving 2,597 patients with gastric cancer were included. Primary meta-analysis indicated a significant association between elevated CRP level and poor OS (HR 1.77, 95% CI 1.56-2.00). Subgroup analyses showed no single factor could alter the primary results when we divided the included studies by "number of patients", "max follow-up period", "TNM stage", "treatment" and "cut-off value". Correlation analyses showed that serum CRP level was significantly related to TNM stage (OR 2.96, 95% CI 2.22-3.93) and tumor recurrence (OR 1.81, 95% CI 1.21-2.71). Conclusions: We demonstrated that increased pretreatment serum CRP level (${\geq}10mg/L$) was significantly associated with poor prognosis in gastric cancer patients, either in early or advanced stages.

• Journal of Gastric Cancer
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• v.3 no.2
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• pp.84-87
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• 2003

Purpose: Evidence exists that dysregulation of Bcl-2 family members is involved in the pathogenesis of cancer development. The aim of this study was to explore whether the somatic mutation of proapoptotic Bcl-2 member genes, one of the mechanisms that prolong the survival of cancer cells, is involved in gastric carcinogenesis. Materials and Methods: In the current study, to detect somatic mutations of the DNA sequences encoding the Bcl-2 homology 3 (BH3) domain of the human BAD, BIM, BIK, and Bcl-G genes in 60 advanced gastric adenocarcinomas, we used the polymerase chain reaction (PCR), single strand conformation polymorphism (SSCP), and DNA sequencing. Results: The SSCP analysis revealed no mutations in the coding regions of the BH3 domain in the cancers. Conclusion: The data presented here indicate that proapoptotic Bcl-2 member genes, BAD, BIM, BIK, and Bcl-G, may not be mutated in human gastric carcinomas and suggest that these genes might be altered by mechanisms other mechanisms somatic mutation.

• Annals of Hepato-Biliary-Pancreatic Surgery
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• v.28 no.1
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• pp.99-103
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• 2024

Pancreatic resections, depending on the location of the tumor, usually require division of the vasculature of either the distal or proximal part of the stomach. In certain situations, such as total pancreatectomy and/or with splenic vein occlusion, viability of the stomach may be threatened due to inadequate venous drainage. We discuss three cases of complex pancreatic surgeries performed for carcinoma of the pancreas at a tertiary care center in India, wherein the stomach was salvaged by reimplanting the veins in two patients and preserving the only draining collateral in one case after the gastric venous drainage was compromised. The perioperative and postoperative course in these patients and the complications were analyzed. None of these 3 patients developed any complication related to gastric venous congestion, and additional gastrectomy was avoided in all these patients. Re-establishment of the Gastric venous outflow after extensive pancreatic resections helps to avoid additional gastric resection secondary to venous congestive changes.

• Journal of agricultural medicine and community health
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• v.26 no.2
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• pp.59-78
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• 2001

Data on reported cancer mortality in the Gyeongsangbuk- do province from 1991 to 1998 were collected and analyzed using the existing mortality reporting system as well as the public health network to furnish accurate data on reported cancer death and to collect data to establish a high quality district health plan. The overall crude death rate in Gyeongsangbuk province in 1991 was 74.56 deaths per 100,000-person but this rate increased to 79.22 in 1998. Among the deaths, the overall death rate of cancer was 16.7% in 1991, which increased to 19.3% in 1998; specifically the death rate of men increased from 19.4% in 1991 to 22.3% in 1998 while that of women increased from 12.4% in 1991 to 15.5% in 1998, showing a more increase among women. The types of cancer and associated death rates in 1991 were gastric cancer(41.5%), followed by liver cancer (28.8%), and lung and bronchogenic carcinoma(8.7%) and in 1998, gastric cancer (24.7%), followed by liver cancer(22.7%), lung and bronchogenic carcinoma(19.3%), showing the same order. For men and women, gastric cancer(40.2% and 44.7%, respectively) was the most common cancer death, followed by liver cancer(33.7% and 16.7%, respectively), and lung and bronchogenic carcinoma(10.2% and 5.0%, respectively) in 1991. However, in 1998, gastric cancer(27.8%) was still the most common type among both men and women, followed by liver cancer (18.5%) and lung and bronchogenic carcinoma(12.7%), showing the most decrease in gastric cancer but most increase in lung and bronchogenic carcinoma. The age- adjusted mortality rates by gastric cancer, hepatoma, laryngeal carcinoma were decreased in both male and female, and also uterine cancer was decreased in female. The age- adjusted mortality rates by lung and bronchogenic carcinoma, pancreatic cancer, rectal cancer were increased in both male and female, and also breast cancer was increased in female. The calculated overall age-adjusted death rate based on the 1995 population was 84.25 in 1991, which decreased to 77.67 in 1998. Male death rate decreased significantly from 119.81 in 1991 to 101.82 in 1998 while the female death rate increased from 48.64 in 1991 to 53.80 in 1998. A census of cancer death rate using accurate death records is important for the establishment of proper and high-quality district health and medical plan and policy. The effort to improve the accuracy of death reports using the health facility network, as had been attempted by this study, can be continued. Furthermore, there must be a way for the Health and Welfare Department to use the death reports to improve the present reporting system. Lastly, additional studies need to be conducted to investigate how much the accuracy was improved by the supplemented death reports in this study.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.11
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• pp.6261-6265
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• 2013

Background: Recent studies have suggested that expression of the RAS protein activator like-1 gene (RASAL1) is decreased in gastric carcinoma tissues and cell lines, indicated a role in tumorigenesis and development of gastric cancer. Reduced expression of RASAL1 could result in aberrant increase of activity of RAS signaling pathways in cancer cells. However, the exact mechanism which induces down-regulation of the RASAL1 gene remains unclear. This study aimed to determine the methylation status and regulation of RASAL1 in gastric cancer. Materials and Methods: Using the methylation-specific polymerase chain reaction (MSP), the methylation status of CpG islands in the RASAL1 promoter in gastric cancers and paired adjacent non-cancerous tissues from 40 patients was assessed and its clinicopathological significance was analyzed. The methylation status of RASAL1 in gastric cancer lines MKN-28, SGC-790l, BGC-823, as well as in normal gastric epithelial cell line GES-l was also determined after treatment with a DNA methyltransferase inhibitor, 5-aza-2'-doexycytidine (5-Aza-CdR). RAS activity (GAS-GTP) was assessed through a pull-down method, while protein levels of ERK1/2, a downstream molecule of RAS signaling pathways, were determined by Western blotting. Results: The frequencies of RASAL1 promoter methylation in gastric cancer and paired adjacent non-cancerous tissues were 70% (28/40) and 30% (12/40) respectively (P<0.05). There were significantly correlations between RASAL1 promoter methylation with tumor differentiation, tumor size, invasive depth and lymph node metastasis in patients with gastric cancer (all P<0.05), but no correlation was found for age or gender. Promoter hypermethylation of the RASAL1 gene was detected in MKN-28, SGC-790l and BGC-823 cancer cells, but not in the normal gastric epithelial cell line GES-1. Elevated expression of the RASAL1 protein, a decreased RAS-GTP and p-ERK1/2 protein were detected in three gastric cancer cell lines after treatment with 5-Aza-CdR. Conclusions: Aberrant hypermethylation of the RASAL1 gene promoter frequently occurs in gastric cancer tissues and cells. In addition, the demethylating agent 5-Aza-CdR can reverse the hypermethylation of RASAL1 gene and up-regulate the expression of RASAL1 significantly in gastric cancer cells in vivo. Our study suggests that RASAL1 promoter methylation may have a certain relationship with the reduced RASAL1 expression in gastric cancer.

• Journal of Gastric Cancer
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• v.1 no.1
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• pp.4-9
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• 2001

Purpose: The trefoil factor family 1 (TFF1) has a protective effect against gastric mucosal damage induced by nonsteroidal anti-inflammatory drugs or ethanol. In addition, a TFF1 knockout mouse model has exhibited circumferential adenomas with high-grade dysplasia, of which $30\%$ progressed into frankly invasive carcinomas. We tried to determine whether the expression pattern of the TFF1 could be involved in the development of sporadic gastric carcinomas. Materials and Methods: We examined TFF1 expression in a series of 43 sporadic gastric carcinomas and 18 gastric adenomas by immunohistochemistry. Results: Strong positive TFF1 staining was identified primarily in the normal gastric mucosa, mainly in the cytoplasm of the superficial and foveolar epithelium. We found TFF1 expression in $55.8\%$ (24 out of 43) of the gastric carcinomas and in $16.7\%$ (3 out of 18) of the gastric adenomas. Statistically, TFF1 immunoreactivity was significantly higher in diffuse-type ($82.4\%$) than in intestinal-type ($38.5\%$) carcinomas(p=0.0058, Fisher's exact test). Conclusion: Our findings provide sufficient evidence that the expression of TFF1 in gastric cancer may simply disclose gastric-type differentiation of neoplastic cells and provide further support for the existence of at least two pathways of malignant transformation of the gastric mucosa: one via intestinal metaplasia and adenomatous dysplasia, leading to glandular carcinomas with intestinal-type differentiation, and the other via hyperplastic changes or de novo changes, leading to diffuse carcinomas and to a subset of glandular carcinomas displaying gastric-type differentiation.

• Journal of Gastric Cancer
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• v.3 no.3
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• pp.151-157
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• 2003

Purpose: In this study, we attempted to ascertain the proton magnetic resonance spectroscopy (${1}^H$ MRS) peak characteristics of human gastric tissue layers and finally to use the metabolic peaks of MRS to distinguish between normal and abnormal gastric specimens. Materials and Methods: Ex-vivo ${1}^H$ MRS examinations of thirty-five gastric specimens were performed to distinguish abnormal gastric tissues invaded by carcinoma cells from normal stomach-wall tissues. High-resolution 400-MHz (9.4-T) ${1}^H$ nuclear magnetic resonance (NMR) spectra of two gastric layers, a proper muscle layer, and a composite mucosasubmucosa layer were compared with those of clinical 64- MHz (1.5-T) MR spectra. Three-dimensional spoiled gradient recalled (SPGR) images were used to determine the size and the position of a voxel for MRS data collection. Results: For normal gastric tissue layers, the metabolite peaks of 400-MHz ${1}^H$ MRS were primarily found to be as follows: lipids at 0.9 ppm and 1.3 ppm; alanine at 1.58 ppm; N-acetyl neuraminic acid (sialic acid) at 2.03 ppm; and glutathione at 2.25 ppm in common. The broad and featureless featureless spectral peaks of the 64-MHz MRS were bunched near 0.9, 1.3, and 2.0, and 2.2 ppm in human specimens without respect to layers. In a specimen (Borrmmann type III) with a tubular adenocarcinoma, the resonance peaks were measured at 1.26, 1.36 and 3.22 ppm. All the peak intensities of the spectrum of the normal gastric tissue were reduced, but for gastric tumor tissue layers, the lactate peak split into 1.26 and 1.39 ppm, and the peak intensity of choline at 3.21 ppm was increased. Conclusion: We found that decreasing lipids, an increasing lactate peak that split into two peaks, 1.26 ppm and 1.36 ppm, and an increasing choline peak at 3.22 ppm were markers of tumor invasion into the gastric tissue layers. This study implies that MR spectroscopy can be a useful diagnostic tool for gastric cancer.