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

Extensive epidemiological and experimental studies have suggested that some chemical agents, nutritional deficiencies, and physical factors are associated with the development of esophageal cancer (EC). Recent evidence also suggests an etiologic role of certain microorganisms in esophageal carcinogenesis either by producing carcinogens or promotors or by acting directly on the host cells. The mutagenic and carcinogenic effects of several fungi and bacteria isolated from the grains and foodstuffs in high-risk areas have been shown by in vitro and in vivo studies. Certain viruses, e.g., human papillomavirus, herpes simplex virus, cytomegalovirus, and Epstein-Barr virus, have been implicated in the pathogenesis of a variety of human cancers, and all of them are known to produce tumors in animals and cell transformation in vitro. These viruses also have been shown to infect the esophageal epithelium. Therefore, although many of the key issues of their mechanisms of action are unclear as yet, they should be considered potential etiologic agents of EC. The present review summarizes the data available on the etiology of EC, emphasizing the current evidence implicating an etiologic role of microorganisms in the pathogenesis of this malignancy.
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PMID:Infectious agents in the etiology of esophageal cancer. 132 35

Retrovirally induced immunosuppression may elevate the incidence of chemically induced cancers. A proposed hypothesis to explain this relationship is the increased free radical activity observed during retroviral infection and carcinogen activation. We previously found that vitamin E retarded growth of esophageal tumors accompanied by reductions of free radical products. This study investigated the contribution that retroviral immunosuppression has on esophageal cancer induced by the carcinogen N-nitrosomethylbenzylamine (NMBzA), and the response that increased levels of dietary vitamin E has on this induced carcinogenesis. Female C57BL/6 mice received NMBzA or vehicle (corn oil) i.p. weekly for 3 weeks. Then some of the mice were infected with LP-BM5 murine retrovirus and fed diets containing 30 IU vitamin E or 172 IU vitamin E/kg of diet. As an assessment of free radical activity, exhaled ethane was measured prior to killing the animals at 26 weeks. Esophagi from the various mice groups were assessed for size and frequency of tumors. Livers homogenates were analyzed for vitamins A and E, lipid fluorescence, conjugated dienes and malondialdehyde. Hepatic levels of vitamin A and E were decreased (P < 0.05) and indices of lipid peroxidation were greater (P < 0.05) in NMBzA-treated mice relative to controls. Lipid peroxidation and serum transaminases (ALT and AST) were greatest in mice given NMBzA and infected with the retroviruses. Incidence of esophageal tumors were also greatest in the NMBzA-treated, immunocompromised animals. Mice fed vitamin E-supplemented diets showed increased (P < 0.05) hepatic concentrations of vitamin E and vitamin A, decreased activities of serum transaminases, decreased indices of lipid peroxidation, and decreased size and frequency of esophageal tumors in both the immunocompromised and non-immunocompromised mice. These results suggest that vitamin E plays an antioxidant function that retards the incidence of esophageal cancers in immunocompromised and non-immunocompromised animals.
Carcinogenesis 1992 Oct
PMID:Vitamin E protection against nitrosamine-induced esophageal tumor incidence in mice immunocompromised by retroviral infection. 133 Mar 43

Humans are exposed to preformed N-nitroso compounds (NOC), but also to a wide range of precursors and nitrosating agents which can react in vivo to form potentially carcinogenic NOC and diazo compounds. Nitrite, nitrate and nitrosating agents can also be synthesized endogenously in enzymic reactions mediated by bacteria, activated macrophages and neutrophils. The latter two cell types generate, via the enzyme nitric oxide synthase, the nitric oxide radical that is involved in cytotoxicity, and is believed to be involved in formation of carcinogenic nitrosamines, DNA base deamination and oxidative damage. Thus endogenous NOC formation, DNA damage and gene mutations in humans could occur at various sites of the body such as the stomach and chronically infected or inflamed organs. Sensitive procedures to estimate the exposure of humans to NOC have been developed and applied in ecological and cross-sectional studies. These have shown that inhabitants of high-risk areas for stomach and esophageal cancer, patients with urinary tract infections (at risk for bladder cancer) and Thai subjects infected with liver fluke (at risk for cholangiocarcinoma) had significantly higher exposure to endogenous NOC. Clinical studies have examined the model of stomach carcinogenesis based on intragastric nitrosation, but the precise roles of bacterial overgrowth and of Helicobacter pylori infection in NOC synthesis and/or inducing oxidative stress in stomach mucosa remain to be clarified. Together these results support the role of NOC and other nitrite-derived mutagens in human cancer etiology, in particular when exposure starts early in life and persists over a long period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endogenously formed N-nitroso compounds and nitrosating agents in human cancer etiology. 133 85

I. Serial histopathologic study of esophageal squamous cell carcinoma. A review of 335 cases of squamous cell carcinoma disclosed 55 cases (16.4%) with glandular components in addition to the ordinary component of squamous cell carcinoma, suggesting that this type of esophageal tumor had originated not only from the covering squamous epithelium but from esophageal gland or ductal epithelium. Intra-epithelial carcinoma concomitant with squamous cell carcinoma was seen in 95 cases (28.4%). The incidences of coexistence in such lesion were higher in the groups of early stage esophageal cancer. These observations support the concept of field carcinogenesis of esophageal cancer. II. Histopathologic study of squamous epithelial dysplasia. Among 91 cases without preoperative treatment, there were 40 dysplastic lesions in 23 cases (25.3%). The continuity of dysplasia to the carcinoma was 48.3% and it was often encountered in severe dysplasia rather than in moderate or mild dysplasia, suggesting some relationship between the severity of dysplasia and carcinoma. III. Immunohistochemical study of EGF and c-myc. Among 27 cases, EGF was positive in 10 (37.0%). c-myc was positive in 18 (66.7%) not only cancer but normal epithelium suggesting that some change of products of oncogene occurred also in the normal epithelium of the patients of esophageal cancer.
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PMID:[Mode of origin of esophageal squamous cell carcinoma--serial histopathologic and immunohistochemical studies]. 147 Jan 59

This paper reports the prevalence of chronic esophagitis and nutritional status among 538 persons 15-26 years old in the high-risk area of esophageal cancer. 166 subjects were from households with history of esophageal cancer while 372 from households without. The frequency of chronic esophagitis among male and female adolescents in the high risk areas (37.6% and 36%) was significantly, higher than that in the low risk areas. Furthermore, the frequency of chronic esophagitis in the adolescents in households with history of esophageal cancer was also higher than that without history of this cancer. There was a positive correlation between avitaminosis C and chronic esophagitis. Suffering from avitaminosis C and B2, these people are prone to develop chronic esophagitis which, in turn, may serve as an early phase in the carcinogenesis of esophageal epithelium.
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PMID:[Preliminary study on nutrition and precancerous lesions of the esophagus in the adolescents]. 161 89

The effects of selenium (Se) concentration and glutathione peroxidase (GSH-Px) activity in the development of esophageal cancer was studied. The results indicated that there were no significant differences in Se level (P greater than 0.2) and GSH-Px activity (P greater than 0.1) in the normal subjects from areas with high and low esophageal cancer mortality. In an area with high esophageal cancer mortality, the Se level and GSH-Px activity of the normal, mild hyperplasia, severe dysplasia and cancer groups decreased gradually. There was a significant difference in the erythrocyte Se concentration of the normal and severe dysplasia groups (P less than 0.03). Erythrocyte Se concentration and GSH-Px activity were significantly lower in the cancer group than in the normal group (P less than 0.001; P less than 0.03). The findings suggest that low erythrocyte Se level and GSH-Px activity were the results of carcinogenesis rather than a cause.
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PMID:[Selenium content and glutathione peroxidase in erythrocytes from different populations in areas with high and low mortality of esophageal cancer]. 180 46

Studies on 7045 metaphase plates in cultured lymphocytes of 40 members from 4 high risk esophageal cancer families in Linxian County are reported. It was found that there were 58 endoreduplication and tetraploid cell appearance in 7045 cells of 18 members out of 40 (45%), with a frequency of 0.82%. Furthermore, 21% of cells with endoreduplication were found in one member of high risk cancer families. Thereupon, we conjecture that these endoreduplication cells may play an important role in the esophageal carcinogenesis in the high risk cancer families in Linxian County.
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PMID:[Genetic etiology of esophageal cancer. VI. Significance of endoreduplication in the cultured lymphocytes from members of high risk cancer families in Linxian County]. 180 47

The rat esophageal carcinogen N-nitrosomethylbenzylamine was shown to be highly toxic to rat esophageal epithelial (REE) cells in short-term primary culture. A significant level of cell killing could be observed at 10(-6) M. Several other esophageal carcinogens were also cytotoxic in a dose-dependent manner. Nitrosamines that do not produce esophageal tumors in the rat were generally unable to kill the esophageal cells. The results demonstrate that REE cells retain their metabolic capacity to activate specific nitrosamines to toxic metabolites. The culture system will be useful for mechanistic studies on the tissue specificity of these carcinogens, as well as to search for environmental agents that kill esophageal cells that may be involved in the causation of esophageal cancer.
Carcinogenesis 1991 Mar
PMID:Selective cytotoxicity of N-nitrosamines to cultured rat esophageal epithelial cells. 200 87

Previous studies have shown that platinum-DNA adduct level in leukocyte DNA (measured by antibody methodology) is directly related to disease response in ovarian cancer and testicular cancer. To determine if this principle could be more broadly applied, platinum-DNA damage was studied in a blinded fashion in leukocyte DNA of 21 cancer patients who received carboplatin (day 1) and cisplatin (day 3) in a phase 1 clinical trial. Fifteen different tumor types were included in this cohort. Using atomic absorption spectrometry with Zeeman background correction, DNA-bound platinum was measured during cycles 1 (C1) and 2 (C2) of therapy for most patients. For each of two cycles of therapy, most patients developed measurable levels of adduct after carboplatin, and in most patients adduct levels increased further after cisplatin, often in a supra-additive fashion. Total mg dose levels varied by less than 2-fold, whereas individual patients differed by as much as 10(3) in their adduct measurements after C1 and after C2, and by 29-fold after the very first carboplatin dose. All patients had refractory disease at the initiation of therapy, and 19 patients were evaluable for disease response. Adduct determinations were made 24 h after the first dose of platinum therapy in 17 of these individuals. Mean adduct levels after the first dose of carboplatin were higher in six responders (50 fmol/micrograms DNA +/- 26) than in 11 non-responders (14 fmol/micrograms DNA +/- 10); Wilcoxon two sample test two-sided P = 0.0071. The six responders were patients with pleural mesothelioma (2), breast cancer, buccal mucosa cancer, esophageal cancer and ovarian cancer. Adduct levels were consistently higher in the group of responders on each day that adduct was measured, with a summary two-sided P value of 0.00011. We conclude that analysis of platinum-DNA adduct formation may help determine whether pharmacogenetics are important in cancer drug resistance; and may help to determine the relationship between DNA damage in the peripheral blood compartment and internal organ response to in vivo exposures to DNA-damaging agents.
Carcinogenesis 1991 Jul
PMID:Platinum-DNA damage in leukocyte DNA of patients receiving carboplatin and cisplatin chemotherapy, measured by atomic absorption spectrometry. 207 Apr 90

Pickled vegetables are a traditional daily food served in several parts of China where esophageal cancer is prevalent, and the mortality rate due to this cancer appears to be correlated with the time span of consumption and the amount consumed. For the present study epithelial hyperplasia and papillomas of the esophagus and forestomach were induced in mice and rats following administration of condensed juice from or extract of pickled vegetables from Linxian County, Henan Province. Only one case of forestomach carcinoma was observed in a rat subsequent to prolonged treatment with pickled extract, indicating that carcinogens in pickled vegetables alone are probably incapable of inducing carcinogenesis.
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PMID:[Studies on pickled vegetables and cause of esophageal cancer in Linxian. I. Experiments on carcinogenicity of pickled vegetables]. 215 91


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