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 studied 112 patients with polyps of the stomach, gallbladder and colorectum by immunohistochemical staining with monoclonal antibody (MG7) against gastric cancer and avidin-biotin complex (ABC) technique. The positive expression of the MG7-corresponding antigen (MG7-Ag) was 100%, 100%, and 60.0% respectively in villous, mixed and tubular polyps. A close correlation was shown between dysplasia of grade II and the positive expression of MG7-Ag (p < 0.05). The positive expression was significantly related to canceration (P < 0.025). No malignancy was found in 45 patients with negative expression. But 12 of 67 patients with positive expression developed cancers in 3 to 38 months. The patients with positive expression of MG7-Ag were high risk group developing cancer.
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PMID:[The expression of MG7 corresponding antigen in gastrointestinal polyps and its relation with cancer]. 133 41

The classification of dysplasias of the gastric mucosa used in our institute includes adenomatous dysplasia, regenerative dysplasia, and cryptal dysplasia. We compared the incidence of gastric dysplasia in three regions of China which have quite different geographical environments: the loess plateau of Wuwei area in the Gansu Province, the island of the Yangtze River in the Jiangsu Province of southern China, and the coastal area of the Liaoning Province in northern China. The mortality rate of stomach cancer in these areas is more than 50 per 100,000. We found a total of 323 cases of gastric dysplasia in these three areas. Regenerative dysplasia is the most common precancerous lesion of the stomach and was found in 40% of the cases from the three high-risk areas of gastric cancer. The background lesions consist of gastric erosions, severe gastritis, gastric ulcers, and intestinal metaplasia, which indicate that some factors causing damage to gastric mucosa are very important in the histogenesis of stomach cancer. The gastric dysplasia sites involved are different in the three geographical regions studied. On the island of the Yangtze River, cardiac dysplasia and intestinal metaplasia are common (75%), and cancer of the cardia is also common. In the other two geographical areas, antral dysplasia predominates (85 to 91%). The finding of different sites of gastric dysplasia in different geographical environments may be very important in our search for etiological factors of gastric cancer and may allow for beneficial intervention in the prevention of this disease.
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PMID:Geographic pathology on the precursors of stomach cancer. 146 19

The anatomic distribution of precancerous gastric lesions among 3,400 residents in Linqu, Shandong Province of China, was compared with the anatomic distribution of stomach cancer (SC) among 959 patients in Tokyo, Japan. The incidence of SC is high in both areas, and locations within the stomach of the precancerous and malignant lesions were classified using similar criteria. Chronic atrophic gastritis (CAG) affected 98% of the population in Linqu, with intestinal metaplasia (IM) the most severe diagnosis in 33% and dysplasia (DYS) in 20%. Neither the SC nor precancerous lesions were uniformly distributed in the stomach. Among the DYS 3% were along the greater curvature of the body, 15% along the lesser curvature of the body, 25% in the angulus, 22% along the lesser curvature of the antrum, and 34% elsewhere in the antrum. Among the SC the corresponding percentages were 2, 16, 28, 25 and 29. The similarity to the SC distribution increased gradually from CAG to IM to DYS, providing further evidence for the multistage progression of precancerous gastric lesions.
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PMID:Comparison of the anatomic distribution of stomach cancer and precancerous gastric lesions. 148 30

The molecular mechanisms of the carcinogenic process of gastric cancer have not been fully understood yet. In order to know whether c-Ha-ras gene is being involved in the process of gastric carcinogenesis, 8 gastric cancer cell lines, 8 cases of gastric cancer and same number of adjacent dysplasia were analyzed for the presence of mutation at codon 12, 13 and 61 of the c-Ha-ras gene by using polymerase chain reaction (PCR) and mutant-specific oligonucleotide hybridization. Point mutations at codon 12 of the c-Ha-ras gene were found in 2 out of 8 gastric cancer and dysplasia samples in one case, but we found no mutation at codon 13 or 61 of the c-Ha-ras gene. These results suggest that the frequency of mutation of the c-Ha-ras gene detected by sensitive PCR technique is low indeed, however it would be notable that such a genetic change has been detected in the dysplastic lesion of the gastric cancer patient.
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PMID:Point mutation at codon 12 of the c-Ha-ras gene in human gastric cancers. 152 24

The stomach cancer develops on dysplastic lesions of gastric mucosa. It can be found in every precancerous condition, as chronic gastritis, gastric adenoma, giant rugal hypertrophy, chronic peptic ulcer, gastric stump after partial resection, pernicious anaemia. So, this dysplastic change is not a specific lesion. Different classifications are known for grading of gastric dysplasia. Authors evaluated them compared with each other. The signs of dysplasia were studied in 306 gastric aimed biopsy specimens from 233 patients between 1979-1990. In this material severe dysplasia occurred in 20.6%. It means a frequency of 0.84% regarding all gastric endoscopies in the same period of time. The endoscopic investigation revealed a protruded lesion in 18.5% and excavated one in 45.9%. What is very important, local change could not be detected in 35.6%. Follow-up study could be performed in 49 patients in a period of 1-7 years. In this group cancer developed in five patients. By the other hand, 22 gastric carcinomas were proved amongst 233 patients. The authors' recommendation is to follow-up the patients bearing gastric dysplasia at least during 10 years after the diagnosis.
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PMID:[Clinical pathology of gastric mucosal dysplasia]. 152 86

A series of 47 human carcinoma cell lines and their cultured cells were examined for human papillomavirus (HPV) genomes with the use of an HPV detection kit (DNA-RNA hybridization, mixed HPV DNA probe of types 6, 11, 16, 18, 31, 33 and 35). Four of 8 cases of mild dysplasia, 3 of 9 cases of severe dysplasia, 3 of 7 cases of carcinoma in situ, 3 of 15 cases of uterine carcinoma and 5 of 6 cases of condyloma acuminatum were shown to contain the HPV DNA genome in primary cultured cells, while HPV was not detected in the third-passage cells except for the three cases of large cell, nonkeratinizing squamous cell carcinoma. HPV was also not detected in such normal tissues as uterine cervical squamous epithelium, uterine cervical columnar epithelium and endometrium. The presence of HPV DNA genomes was detected consistently in the passages of three lines (SKG-II, HKMUS and HKTUS; large cell nonkeratinizing squamous cell carcinomas of the uterine cervix) with the use of the Southern Blot method (DNA-DNA hybridization, mixed HPV probe of types 6, 11, 16 and 18). HPV type 16 DNA was detected in HKTUS, and HPV type 18 DNA was found in SKG-II and HKMUS. The other 44 cell lines, including ovarian carcinoma, endometrial carcinoma, sarcoma, gastric cancer, pancreatic cancer and rectal cancer, were negative for the HPV-6, HPV-11, HPV-16, HPV-18, HPV-31, HPV-33 and HPV-35 genomes under stringent hybridization conditions.
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PMID:Presence of human papillomavirus genome in human tumor cell lines and cultured cells. 166 88

Overexpression of the Multiple Drug Resistance gene (MDR1) has been proposed as a major mechanism related to both intrinsic and acquired resistance to chemotherapeutic agents. The gene product is a membrane protein (P-glycoprotein), that acts as an energy-dependent drug efflux pump decreasing drug accumulation in resistant tumor cells. We have characterized MDR1 and P-Glycoprotein expression in human gastric adenocarcinoma and in precursor lesions. MDR1 mRNAs, analyzed by dot-blot technique, were detected in 9 of 10 non-tumoral gastric mucosae and in 8 of 10 gastric adenocarcinomas. Immunohistochemical analysis, using the MRK16 monoclonal antibody, revealed heterogeneous expression of P-Glycoprotein in individual cells. The P-Glycoprotein was found on the surface of cells of gastric areas with intestinal metaplasia subtype III. This type of intestinal metaplasia, also called "colonic metaplasia", has been strongly associated with a high risk for the development of gastric cancer. The fact that the P-Glycoprotein was detected in this precursor lesion is consistent with the intestinal metaplasia-dysplasia and carcinoma sequence proposed in the histogenesis of this tumour. The finding that P-Glycoprotein was heterogeneously expressed in malignant cells of some gastric adenocarcinomas also suggests that this transporter system probably contributes to primary and secondary multidrug resistance in this neoplasm.
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PMID:Multidrug resistance gene and P-glycoprotein expression in gastric adenocarcinoma and precursor lesions. 167 10

Surgical specimens from 2 patients with chronic ulcerative colitis accompanied with colon cancer were evaluated by immunoperoxidative staining using monoclonal antibodies A7 (against human colon cancer), S202 (against human gastric cancer), and anti-carcinoembryonic antigen (CEA). The three monoclonal antibodies were reactive with cancerous tissue, anti-CEA antibody and monoclonal antibody S202 reacted with dysplasia tissues, whereas monoclonal antibody A7 did not. Using high-iron diamine technique for mucosubstances (sialomucin and sulfomucin), cancer and dysplasia showed no secretory elements. Surrounding mucosa showed both sialomucin and sulfomucin secretion.
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PMID:[Two cases of ulcerative colitis with colon cancer: immunoperoxidase staining using monoclonal antibodies against gastrointestinal tumor and mucin staining]. 169 18

To explore the dynamics of the progressive loss of cell differentiation observed in the gastric precancerous process, the abnormal expression of Lea antigen in the gastric epithelium was investigated. Gastric biopsy specimens of 122 subjects with Le(a-b+) phenotype who had intestinal metaplasia of the gastric mucosa were studied. The subjects are residents of a rural area in the Colombian Andes with very high risk of gastric cancer. The abnormality was detected with increasing frequency in lesions with other markers of progression of the precancerous process, namely, colonic-type of morphology of the metaplastic cells, expression of sulfomucins, and dysplastic changes. The concomitant expression of the abnormal Lea antigen and sulfomucins was found to be a more reliable marker of more advanced lesions such as colonic metaplasia and dysplasia than either marker alone.
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PMID:Lewis antigen alterations in gastric cancer precursors. 173 13

It has been hypothesized that bacterially produced N-nitroso compounds cause the progression from chronic atrophic gastritis through intestinal metaplasia and dysplasia to gastric cancer. If this is true then various consequences follow. These consequences are discussed, together with the evidence for or against them. The conclusion is that there is much to support the hypothesis.
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PMID:Bacterial N-nitrosation and gastric carcinogenesis in humans. 174 96


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