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Query: UMLS:C0546837 (esophageal cancer)
8,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The coexistence of a benign tumor and carcinoma in the same esophagus is uncommon, while the occurrence of carcinoma in the surface epithelium over a benign tumor is considered to be extremely rare. Among 587 patients with surgically resected esophageal cancer, the cases with carcinoma located over a benign tumor of the esophagus were histopathologically investigated and the carcinogenesis of such cases was discussed. Only three cases were found to have esophageal squamous cell carcinoma located over benign tumors (two were leiomyomas and one was a lipoma). All three benign tumors protruded to the esophageal surface, and the carcinoma was located just over such tumors without coexisting epithelial dysplasia. Moreover, the epithelium, except for portions around these tumors, was intact in all three cases. From these findings it was suggested that chronic stimulation of the epithelium covering the benign tumors might have induced the carcinoma.
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PMID:Esophageal squamous cell carcinoma occurring in the surface epithelium over a benign tumor. 763 Jan 76

The mutation and deletion of APC, MCC genes in human esophageal cancer were analyzed by PCR amplification and direct sequencing assay. In PCR amplification analysis, one of 10 cases of esophageal cancer was found to have APC gene deletion in exon 11; one of 10 cases of EC was found to have MCC gene deletion in exon 12; one case of EC was found to have MCC gene deletion in exon 12. One of adjacent non-tumor tissue was also found to have deletion at exon 12 of MCC. In PCR direct sequencing analysis, two of 10 cases of EC were found to contain APC gene mutation in exon 11, two of 7 cases of EC were found to contain MCC genes mutation in exon 12. The results confirmed that mutation of APC and MCC genes exists in human esophageal cancer. It gives new clues to the understanding of carcinogenesis of human esophageal cancer. The mechanism of mutation or deletion of APC and MCC genes in EC needs further study.
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PMID:[Mutation of tumor suppressor genes APC and MCC in human esophageal cancer]. 765 96

Results of epidemiological studies have shown that nitrosamine-induced carcinogensis is involved in esophageal cancer in China. In order to demonstrate the mechanism at molecular level, Multiple tumor suppressor genes Rb, p53, APC and MCC in human fetus esophageal epithelium treated with NMBzA (in vitro) for 24 hours or three weeks and esophageal carcinoma induced by NMBzA were analyzed with PCR amplification and direct sequencing. In PCR amplification analysis. Rb, p53, APC and MCC deletions in esophageal carcinoma of human fetus induced by NMBzA were found, but no deletions of these genes was demonstrated in NMBzA-treated human fetal esophageal epithelium. PCR direct sequencing analysis revealed mutation of p53, Rb and MCC genes in human fetal esophageal epithelium treated with NMBzA for three weeks. The results first confirmed (in vitro) that nitrosamine can cause mutations and deletions of multiple tumor suppressor genes in human esophageal epithelium. The mutations of tumor suppressor genes in nitrosamine-induced esophageal carcinoma may occur in the early stage, while deletions in late stage of carcinogenesis.
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PMID:[Multiple tumor suppressor genes in esophageal carcinoma induced in human fetus esophageal epithelium by NMBzA]. 765 18

Fusarium moniliforme (FM) is a major fungal pathogen of corn and is involved with stalk rot disease. FM is widely spread throughout the world, including the United States. Most strains of FM produce several mycotoxins, the most prominent of which is called fumonisin. Recent epidemiological studies indicated that ingestion of fumonisin correlates with a higher incidence of esophageal cancer in Southern and Northern Africa and China. Furthermore, fumonisin causes a neurodegenerative disease in horses, induces hepatic cancer in rats, and induces pulmonary edema in swine. Considering that high levels of fumonisin have been detected in healthy and diseased corn grown in the United States, fumonisin may pose a health threat to humans and livestock animals. Structurally, fumonisin resembles sphingolipids which are present in the membranes of animal and plant cells. At the present time, very little is known concerning the mechanism by which fumonisin elicits its carcinogenic effect. Our studies indicate that fumonisin represses expression of protein kinase C and AP-1-dependent transcription. In contrast, fumonisin stimulated a simple promoter containing a single cyclic AMP response element. Since fumonisin did not alter protein kinase A activity, it appears that cyclic AMP response element activation was independent of protein kinase A. It is hypothesized that the ability of fumonisin to alter signal transduction pathways plays a role in carcinogenesis.
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PMID:Repression of protein kinase C and stimulation of cyclic AMP response elements by fumonisin, a fungal encoded toxin which is a carcinogen. 771 70

We examined the expression of cyclin D1 mRNA in two human carcinoma cell lines (A431 and TT) and 17 specimens of esophageal cancer with in situ hybridization. Cyclin D1 mRNA was overexpressed in the cytoplasm of cancer cells that showed cyclin D1 gene amplification by Southern blot hybridization. Cyclin D1 antigen was overexpressed in the nucleus of these cancer cells. The distribution of cyclin D1 mRNA-positive cells was similar to that of cyclin D1 antigen-positive cells in the cancer tissues. We then attempted to correlate overexpression of cyclin D1 antigen and prognosis, by using 55 formalin-fixed, paraffin-embedded specimens of esophageal cancer. The overall 5-year survival of patients with strongly staining tumors was significantly lower than that of patients with weakly or nonstaining tumors (7 versus 59%; P < 0.01). There was no significant correlation between cyclin D1 expression and other clinicopathological factors. These results suggest that cyclin D1 may play an important role in carcinogenesis and that cyclin D1 overexpression may be a useful prognostic factor in esophageal cancer.
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PMID:Overexpression and localization of cyclin D1 mRNA and antigen in esophageal cancer. 774 10

Mutations of ras oncogene and multiple tumor suppressor genes p53, Rb and APC in esophageal epithelium of rhesus monkey fed with one dose of N-methyl-N-benzylnitrosamine (NMBzA 30mg/kg), which was found in high incidence areas of esophageal cancer in China, were analysed by PCR and direct sequencing. Mutation at codon 12 of Ha-ras gene was not found in esophageal epithelium of monkey fed with NMBzA. Some mutations of p53 gene were found in esophageal epithelium of monkey after being fed with NMBzA for 24-48 hours. Some mutation of Rb and APC were found in esophageal epithelium of monkey after being fed with NMBzA for 48 hours. The mutation fingerprints of these genes disappeared in esophageal epithelium of monkey after being fed with NMBzA for 5 days. The results demonstrated that chemical carcinogen NMBzA can induce mutations of multiple tumor suppressor genes in monkey (in vivo) and indicated that the alteration of tumor suppressor genes in the initial stage of carcinogenesis needs many hits by chemical carcinogen. These alterations of p53, Rb, APC genes were similar to the changes of these genes in some reported previously primary esophageal cancer.
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PMID:[Effect of NMBzA on the oncogene and multiple tumor suppressor genes in monkey esophageal epithelium]. 778 Nov 21

To study the role of hot mate drinking, alcohol, tobacco, and diet in esophageal cancer, a case-control study including 131 cases and 262 hospital controls was carried out in La Plata, Argentina. In multivariate analyses, statistically significant increases in risk were detected for alcohol, tobacco, and some dietary factors but not for hot mate drinking. A strong dose-response relationship was observed with the amount of alcohol consumed daily but not with the number of cigarettes smoked. The odds ratio for those drinking more than 200 ml of ethanol/day compared to nondrinkers was 5.7 (95% confidence interval, 2.2-15.2). An increased risk was also observed for those eating barbecued meat more than once a week (odds ratio, 2.4; 95% confidence interval, 1.2-4.8) as compared to those eating it less than once a week, and a reduction in risk was associated with daily consumption of nonbarbecued beef as compared to those eating it less than daily. Concerning mate drinking, the only variable that showed an effect was the temperature at which mate is drunk. Those who reported drinking mate hot or very hot as compared to those drinking it warm had an increase in risk (odds ratio, 1.7; 95% confidence interval, 1.0-2.9). Our findings strengthen the evidence for an important role of alcohol and tobacco in esophageal carcinogenesis but do not provide strong support for a role of hot mate drinking.
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PMID:Alcohol, tobacco, diet, mate drinking, and esophageal cancer in Argentina. 782 85

p53 gene in human esophageal cancer (EC) and cancer of gastric cardia was analyzed. Southern blotting hybridization revealed that five of 35 of EC sample were found to contain abnormal structure of p53 gene, including 2 deletions and 3 rearrangements; two of 27 adjacent non-tumor tissues also contain abnormal structure of p53 gene (7.4%), among them one case was fragment deletion and another case was rearrangement. PCR-direct sequencing technique was used to detect p53 point mutation within exon and intron 5 through 9. Fifteen of 30(50%) of esophageal squamous cell carcinomas contained mutation of p53 gene. Five of 11(45%) adjacent non-tumor tissues also contained mutation of p53 gene. An esophageal adenocarcinoma showed p53 mutation. Three of 4 carcinoma of gastric cardia showed p53 mutation. Mutation spectrum in EC: 8 of 22 cases (36.4%) of p53 mutation were G:C to A: T transition, 6 of 22 cases (27.3%) of p53 mutation were frameshift mutation, including 13.6% (3/22) insertion and 9.1% (2/22) deletion mutation. Some new sites of p53 mutation in human EC were identified. The results suggest that the p53 gene plays an important role in carcinogenesis of human esophagus and gastric cardia.
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PMID:[Mutation of p53 gene in human cancers of the esophagus and gastric cardia]. 795 92

The mutation and deletion of the multiple tumor suppressor genes, including p53, Rb, APC and MCC in the same tissue of humanesophageal cancer (EC) and adjacent non-tumor were analysed by PCR amplification and direct sequencing. In 10 cases of EC 6 were found mutations of p53 gene, 5 were found abnormality of Rb gene, 3 were found mutation of APC gene, 3 were found mutation of MCC gene, 8 were found atleration abnormality of tumor suppressor genes Rb, p53, APC and MCC, 6 were found two or more abnormality of the tumor suppressor genes. The results indicated that the alterations in multiple of tumor suppressor genes were related to carcinogenesis of human esophageal cancer.
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PMID:[The multiple tumor suppressor genes in human esophageal cancer]. 799 60

Abnormalities of epithelial proliferation have been proposed as an early step in gastrointestinal carcinogenesis. To determine whether micronutrient supplementation may reduce squamous epithelial proliferation in the esophagus, we evaluated proliferation in subjects participating in a randomized nutrition intervention trial in Linxian, China, where esophageal cancer rates are among the highest in the world. After 30 months of intervention involving daily supplementation with multiple vitamins and minerals, an endoscopic survey was performed and squamous biopsies from 512 subjects were labeled with tritiated thymidine and autoradiographed. Analysis showed no treatment effect on the overall amount of squamous epithelial proliferation measured by the total labeling index. However, a measure of the vertical distribution of labeled cells showed lower values with supplementation: a 14% reduction in all subjects (P = 0.29), and a 29% reduction in nonsmokers (P = 0.03). These results suggest a potential modest benefit for short-term intervention with multiple vitamins and minerals on squamous epithelial cell proliferation of the esophagus in this high-risk population.
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PMID:Effects of vitamin/mineral supplementation on the proliferation of esophageal squamous epithelium in Linxian, China. 801 79


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