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

Histopathologic and tritiated thymidine labelled autoradiography was carried out on 206 human esophageal biopsy specimens obtained in Linxian county, a high risk area of esophageal cancer in China. According to the histopathologic criteria, 6 cases showed atrophy, 151 normal, 31 hyperplasia, 14 dysplasia and 4 carcinoma. The index of labeled cells were: atrophy 3.3, normal 4.73, hyperplasia 4.9, dysplasia 5.6, carcinoma in situ 11.76 and invasive carcinoma 24.63. Significant increase in labeling was found in the esophageal mucosa with hyperplasia, dysplasia and carcinoma. There was a gradient of increased expansion in the basal layer as the proliferating cells progress from normal to hyperplasia, to dysplasia, and to carcinoma. These results show that the hyperplastic and dysplastic cells were fundamental phases of carcinomatous change in the esophageal mucosa. It shows a wide spectrum of cellular alterations in the course of malignant change and the close relationship between the morphological alterations and cell biology.
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PMID:[Histogenesis of esophageal carcinoma]. 139 60

Squamous cell carcinoma is the most common malignant tumor of the esophagus and it is one of the most common fatal cancers worldwide. There is great geographic variation in occurrence of these tumors. Especially high-risk areas have been identified in Northern Iran, Central Asian Republics, Northern China and South Africa. In some of these areas annual mortality rates reach 133/100,000 and over 20% of the population dies of esophageal cancer. The mortality in the US is considerably lower (3 to 8 per 100,000). In common with squamous dysplasias elsewhere eg the cervix, squamous dysplasia of the esophagus also appears to be a precancerous lesion. We have found that squamous dysplasia and early cancer are characterized by a number of distinctive endoscopic changes, namely, mucosal friability, erosions, plaques and nodules. Another finding of interest is the failure on our part to confirm the frequency of esophagitis in high risk areas. Barrett's esophagus is an epithelial metaplasia which replaces esophageal squamous epithelium for variable lengths from the lower esophageal sphincter region cephalad. It is a complication that occurs in approximately 12% of patients with prolonged gastroesophageal reflux. The importance of this disorder is that it is associated with an increased risk of adenocarcinoma of the esophagus. In assessing biopsies from patients with Barrett's esophagus, the main role of the pathologist is to be on the alert for histologic features of dysplasia and adenocarcinoma. Since dysplasia in Barrett's is endoscopically invisible, multiple biopsies are necessary if surveillance is to be successful in detecting dysplastic lesions and early carcinoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Malignant and premalignant lesions of the esophagus. 143 13

The notion that requirements for folic acid may be higher in some tissues than others, resulting in localized deficiencies in spite of blood levels in the normal range was first suggested by the observation of megaloblastic changes in the cervical epithelium that responded to folate supplementation. Theoretically, such deficiencies may arise from elevated folate turnover in response to rapid tissue proliferation or repair; inactivation or alteration of its function by external agents such as tobacco, alcohol, or drugs; or altered metabolism or tissue uptake caused by an inborn error. Marginal dietary intake could aggravate these effects on cells at risk. Evidence for the possible existence of localized folate deficiencies in the aerodigestive tract includes lower circulating folate levels in smokers as compared with nonsmokers; yet lower circulating levels in smokers with bronchial metaplasia; lower folate levels in scrapings of the buccal mucosa of smokers than non-smokers; apparent improvement in bronchial atypical metaplasia in smokers supplemented with folic acid; lower erythrocyte folate levels and higher prevalence of cellular features compatible with folate deficiency in geographic areas and individuals in South Africa at high risk for esophageal cancer; and a trend toward a lower prevalence of colonic dysplasia in ulcerative colitis patients who use folic acid supplements. These observations, as well as animal and in vitro studies, also suggest that folate deficiency may be co-carcinogenic. Further research in this area will be aided by the development of animal models of localized folate deficiency and of methodologies capable of measuring folate levels in minute quantities of tissues and exfoliated cells.
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PMID:Localized deficiencies of folic acid in aerodigestive tissues. 144 61

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

Balloon-mesh cytologic screening for esophageal cancer done in 255 asymptomatic high-risk United States veterans (age greater than 40 years, ethanol abuse for greater than 20 years, and cigarette smoking greater than 20 pack years) identified 37 patients with squamous cell dysplasia. Of the 37 patients with dysplasia, 28 were re-evaluated prospectively at 6-month intervals for up to 36 months by balloon-mesh cytology, esophagoscopy with vital staining and biopsies, chest radiographs, oropharyngeal examination, and indirect laryngoscopy. During prospective follow-up evaluation, cytology specimens were repetitively normal in 16 patients (57%), showed inflammatory changes in eight patients (29%), persisted as dysplasia in two patients (7%) (both had endoscopic and histologic evidence of esophagitis), and progressed to carcinoma in two patients (7%) (one esophageal, one laryngeal). Although histologic findings concurred with the resolution of dysplasia, biopsy specimens were characterized by a similar difficulty in distinguishing dysplasia from inflammation. Erroneous histologic diagnoses of carcinoma in situ were made in two patients with reflux esophagitis evident endoscopically and confirmed during the course of a 24-36 month follow-up period. The authors conclude that squamous cell dysplasia detected by balloon-mesh cytology is seldom a precursor of esophageal cancer in the high-risk U.S. population but, rather, is often related to esophagitis. Thus, balloon-mesh cytology has limited use as a screening method for the early detection of esophageal cancer in the United States.
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PMID:Natural history and significance of esophageal squamous cell dysplasia. 169 60

Oncologic screenings of the populations in the areas with increased incidence of esophageal cancer have revealed Barrett's ulcer in 1 percent of the examinees. Endoscopic and cytologic characteristics of this condition are presented. Precancer changes--severe dysplasia--are most frequent in male Kazakhs (14.1 percent) aged 50 to 59 (14.7 percent). Subjects with Barrett's ulcer developing severe dysplasia, as evidenced by cytograms, should be included in the group of subjects at risk for carcinoma of the lower third of the esophagus and cardia.
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PMID:[Cytologic criteria for the formation of a risk group in Barrett esophagus]. 170 83

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

9633 subjects aged 40 to 65 were sampled from high-risk areas for esophageal cancer and examined by esophageal exfoliative cytology. 2531 and 3393 cases of markedly and mildly dysplastic patients were screened out respectively. Those with marked dysplasia were randomized into 3 groups and given respective medications: antitumor B (Chinese herbs), 4-ethoxycarbophenylretinamide (retinamide) and placebo. The subjects with mild dysplasia were randomly divided into 2 groups for riboflavin and placebo treatment. After medication for 3 or 5 years the subjects were reexamined by esophageal exfoliative cytology. The incidence of esophageal cancer in the antitumor B group after taking medication for 3 and 5 years was reduced by 52.2% and 47.3% respectively as compared with the placebo group. These differences were statistically significant (chi 2 = 8.9115, P less than 0.01; chi 2 = 10.9573, P less than 0.01). The incidence of esophageal cancer in the retinamide group after 3 years of medication was reduced by 37.3% as compared with control, while the incidence among patients treated for 5 years dropped by 43.2% relative to control. This difference was statistically significant (chi 2 = 9.2836, P less than 0.01). The incidence of esophageal cancer in the riboflavin group was reduced by 22.2% and 34.8% respectively. The above results indicate that secondary prevention of esophageal cancer is possible and that inhibitory therapy of precancerous lesions of the esophagus is effective in preventing esophageal cancer. This method needs further trial and study in high risk areas of esophageal cancer. The reliability of the experimental results is critically discussed.
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PMID:[Medicamentous inhibitory therapy of precancerous lesions of the esophagus--3 and 5 year inhibitory effect of antitumor B, retinamide and riboflavin]. 214 82

A series of 51 biopsies derived from the same number of patients with established invasive squamous-cell carcinoma of the esophagus in Linxian, a high-risk area for esophageal cancer in China, were analyzed histologically and by in situ DNA hybridization to demonstrate human papillomavirus (HPV) infection. Epithelial changes suggesting HPV infection within or adjacent to the carcinoma lesions were found in 25 cases (49.0%). Esophageal lesions with HPV morphology showed both flat (25 cases) and inverted condylomas (2 cases) resembling those found in the genital tract. HPV 6, 11, 16 or 18 DNA sequences were detected in 22/51 (43.1%) of the esophageal specimens. HPV DNA was most frequently localized in epithelium adjacent to carcinomas in areas showing either epithelial hyperplasia (36.1%) or dysplasia (22.2%). Of the lesions with morphological HPV changes, 64% (16/22) were shown to contain HPV DNA. In 2 specimens, HPV DNA was found in frankly malignant cells. High-risk types HPV 16 and/or 18 DNA sequences were found in 16 of the 22 HPV DNA-positive cases (72.7%). Our results confirm previously reported HPV involvement in esophageal squamous-cell lesions, and support the hypothesis of HPV as a possible etiological agent in esophageal carcinogenesis.
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PMID:Human papillomavirus (HPV) DNA in esophageal precancer lesions and squamous cell carcinomas from China. 215 38

A series of 80 esophageal cytologic specimens derived from the same number of patients with previously diagnosed squamous cell dysplasia of the esophagus were examined for the presence of human papillomavirus (HPV) infection by filter in situ hybridization (FISH), using a mixed DNA probe containing HPV types 11, 16, and 18. All the patients came from an area at high risk for esophageal cancer in China. A total of 53 cases (66.3%) were demonstrated as HPV-DNA-positive. HPV DNA was detected in 22.2% (2 of 9) of the patients without cytologic atypia, in 50% (3 of 6) with mild dysplasia, in 80.6% (25 of 31) with moderate dysplasia, in 67.9% (19 of 28) with severe dysplasia, and in 66.7% (4 of 6) with an invasive squamous cell carcinoma. The present results confirm the recent findings on HPV involvement in esophageal squamous cell lesions. They support the hypothesis that HPV is a possible etiologic agent in esophageal carcinogenesis, most probably acting synergistically with physical, chemical, and/or nutritional factors that have previously been related with this malignancy in the high-risk areas of China.
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PMID:Detection of human papillomavirus DNA in cytologic specimens derived from esophageal precancer lesions and cancer. 215 55


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