Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Esophagus from adult male CDF rats was cultured for a period of 28 d in CMRL-1066 medium supplemented with pyruvic acid, HEPES buffer, beta-retinyl acetate, and antibiotics. Morphological, radioautographic, and biochemical studies indicated that the survival of the tissue in serum-free medium was equivalent to that in medium containing 5% heat-inactivated fetal bovine serum. There was a relatively constant uptake of [3H]thymidine into DNA and [3H]leucine into protein of the esophageal explants during the incubation. Only the basal cells of the epithelium incorporated [3H]thymidine into their nuclei. The normal morphology of the tissue was preserved when the explants were maintained at both 37 and 30 degrees C, and in either 50 or 20 % 02. Ninety-five percent O2 was highly toxic to the cells of the explants. This culture system should be suitable for a variety of investigations in esophageal cell differentiation and carcinogenesis.
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PMID:Explant culture of rat esophagus in a chemically defined medium. 732 97

Helicobacter pylori (HP) plays a crucial role in gastric carcinogenesis. Few studies have looked at the relationship between HP and Barrett's esophagus/cancer. To further investigate this, a study comparing the prevalence of HP and increasing grades of dysplasia was undertaken. Biopsies from 19 malignant and 94 benign cases of Barrett's esophagus were analysed histologically for the presence of HP. 34% of non-dysplastic Barrett's epithelium was colonized with HP compared with only 17% of dysplastic/malignant cases (P = 0.04). No relationship was found between HP status and: (i) length of Barrett's esophagus; (ii) the presence of ulcers or strictures; and (iii) previous anti-reflux surgery. HP colonization of Barrett's esophagus is not uncommon. We found that HP has a negative correlation with increasing dysplasia which is analogous to gastric carcinogenesis. This finding should be investigated in prospective studies to elucidate its role in Barrett's adenocarcinoma.
Dis Esophagus 1997 Jul
PMID:Helicobacter pylori colonization of Barrett's esophagus and its progression to cancer. 928 79

The present study was undertaken in order to investigate the possible involvement of high-risk human papillomavirus (HPV; types 16 and 18) or the overexpression of p53 protein in 123 Japanese patients with esophageal squamous cell carcinoma (SCC) from five different institutions. We detected HPV DNA in 30.1% (37/123) by in situ hybridization (ISH). Of these 123 cases, HPV type 16 was detected in 22 cases and HPV type 18 in 23 cases. In addition, HPV types 16 and 18 were detected simultaneously in eight cases. We found an almost similar incidence of HPV infection at five different places in Japan. Then, among these patients, 24 fresh tumor samples were also examined for screening the presence of HPV DNA using dot blot hybridization (DBH) and polymerase chain reaction (PCR). We detected HPV DNA in 20.8% (5/24) by DBH and in 12.5% (3/24) by PCR. P53 protein overexpression was found in 34.1% (43/123) by immunohistochemistry (IHC). Furthermore, in 43 cases from Kochi Medical School, the group positive for p53 antibody statistically showed worse survival rate than the group negative for both HPV DNA and p53 antibody. Judging from these results obtained in the present study, HPV infection and p53 overexpression are frequently detected and involved in the carcinogenesis of esophageal SCC in Japan. We also found that no significant geographical difference of both HPV infection and p53 overexpression of esophageal SCC was seemingly present in Japan.
Dis Esophagus 1998 Jul
PMID:High-risk human papillomavirus infection and overexpression of p53 protein in squamous cell carcinoma of the esophagus from Japan. 984 97

It is known that some nitrosamines preferably affect particular organs because of their organospecificity. Diethylnitrosamine (DEN) is one of the most powerful nitrosamines for experimentally inducing esophagus cancer. The present study aimed to evaluate the rate and type of epithelial lesions induced by DEN in mice. We also assessed the role of alcohol and N-nitrosonornicotine (NNN) as promoters of this carcinogenesis. A total of 208 female mice (Mus musculus) were allocated to five experimental groups: group 1, water only (controls); group 2, DEN + water; group 3, DEN + NNN; group 4, DEN + 6% alcohol solution; group 5, DEN + NNN + 6% alcohol solution. Animals in groups 2, 3, 4 and 5 received DEN (0.04 ml/l) three times per week, and during the following 4 days they received the other solutions. NNN was provided at a final concentration of 30 mg/l. The overall experimental period was 180 days. At the end of this time, the animals were killed and their esophagus was dissected for macro- and microscopic analysis. There was no significant difference in relation to the size of the esophagus and to the average DEN intake by the animals (p > 0.05). A statistically significant difference (p < 0.0001) was observed between controls and all other experimental groups. There was no significant difference among experimental groups treated with carcinogens (p > 0.05). The average incidence of cancer was 85.4%. The experimental model used in the present study is a very potent indicator of esophagus cancer. Owing to the high incidence for cancer observed in the present study, it was not possible to assess the effect of alcohol and NNN as inducers for the development of esophageal cancer.
Dis Esophagus 1999
PMID:Induction of esophageal carcinogenesis by diethylnitrosamine and assessment of the promoting effect of ethanol and N-nitrosonornicotine: experimental model in mice. 1046 41

Studies in human beings and animals have shown that esophageal exposure to duodenal and gastric contents may be important for the development of Barrett's esophagus and its complications, including adenocarcinoma and epidermoid carcinoma. Diethylnitrosamine (DEN) is a carcinogen that stimulates the development of epidermoid carcinoma in the esophagus of mice. The aim of this study was to evaluate the effect of gastroduodenal and gastric content reflux on induction of esophageal carcinogenesis. Gastroesophageal reflux (GER) and gastroduodenoesophageal reflux (GDER) were produced by cardioplasty and esophagoduodenostomy. The chosen carcinogen was DEN, diluted in drinking water, given 3 days a week for 20 consecutive weeks. One hundred Wistar female rats were divided into six groups, as follows: group 1 (18 rats), cardioplasty without DEN; group 2 (18 rats), cardioplasty with DEN; group 3 (10 rats), only water; group 4 (17 rats), cardioplasty with DEN; group 5 (17 rats), esophagoduodenostomy with DEN; group 6 (20 rats), only DEN. GER in isolation induced papillomatosis or ulceration in 22.2% of rats and, when associated with DEN, induced papillomatosis in 61.1% of rats. GDER in isolation induced marked esophagitis in 61.1% of rats, Barrett's esophagus in 16.7% and esophageal adenocarcinoma in 16.7%; when associated with DEN, 23.5% of rats presented marked esophagitis, papillomatosis or ulceration, whereas 76.5% had esophageal carcinoma, with 70.6% epidermoid carcinoma and 5.9% adenocarcinoma. Rats treated with water alone did not show histologic abnormalities of the esophageal mucosa. Rats treated with DEN alone developed papillomas in 50.0% of the cases and remained histologically unchanged in 50.0%. There was no development of low- or high-grade dysplasia in any group. The conclusions are that (1) GDER is significantly more deleterious to esophageal mucosa than GER; (2) in this study, GER did not present carcinogenic potential in relation to the esophagus; (3) GDER in isolation is an esophageal carcinogen, producing Barrett's esophagus and esophageal adenocarcinoma; (4) esophageal oncogenesis caused by GDER is potentiated by DEN, inducing esophageal epidermoid carcinoma; (5) in this study, DEN in isolation did not generate tumors in the esophagus of rats.
Dis Esophagus 1999
PMID:Influence of surgically induced gastric and gastroduodenal content reflux on esophageal carcinogenesis--experimental model in Wistar female rats. 1046 42

It is generally accepted that patients with squamous cancers of the esophagus are known to have a high risk of concomitant head and neck cancer. However, there have been only a few reports describing microsatellite instability (MSI) in patients with both esophageal squamous cell carcinoma and head and neck cancers. To evaluate the role of genetic instability in carcinogenesis in such patients, we analyzed six microsatellite loci in 21 tumors from 10 patients who had developed primary cancers of both the esophagus and the head and neck. MSI was detected in 6 out of 10 patients. In five patients with double cancer, MSI was observed at the same microsatellite loci in both the esophageal and the head and neck tumors obtained from the same individuals. These data suggest that such patients may have the same underlying defect in the mismatch repair system, providing insight into possible mechanisms for field carcinogenesis.
Dis Esophagus 1999
PMID:Microsatellite instability in double cancers of the esophagus and head and neck. 1046 46

The modifying effects of phytic acid and gamma-oryzanol on the promotion stage of carcinogenesis were investigated using several two stage carcinogenesis models in rats. In a multi-organ carcinogenesis model, male F344 rats were given combined treatment with 2,2'-dihydroxy-di-n-propylnitrosamine (DHPN), N-ethyl-N-hydroxyethylnitrosamine (EHEN) and 3,2'-dimethyl-4-aminobiphenyl (DMAB) during the initial 3 weeks as initiators, and then treated with dietary 2% phytic acid (50% in water), 1% gamma-oryzanol or basal diet alone for 32 weeks. Although the appearance of hepatic tumors was suppressed, the incidence of urinary bladder papillomas was increased by phytic acid. In addition, the incidence and multiplicity of lung tumors were significantly increased by gamma-oryzanol. Esophagus, colon, pancreas, kidney and thyroid lesion development was not influenced by these compounds. In a gamma-oryzanol dose response experiment using DHPN in the drinking water as an initiator, enhancing effects on lung were observed at a dose of 1% but not at 0.5% or lower. When the modifying effects of phytic acid, and its sodium (Na-PA), potassium (K-PA) and magnesium (Mg-PA) salt were further examined in rats pretreated with the bladder carcinogen N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN), a clear increase in the incidences of bladder tumors was noted, with only Na-PA, phytic acid itself being without effect. Finally, examination of the modifying potential of phytic acid and gamma-oxyzanol on mammary carcinogenesis in female Sprague Dawley rats pretreated with a single intragastric dose of 7,12-dimethylbenz(a)anthracene (DMBA) revealed no significant differences in the final incidences and multiplicities of mammary tumors, but the average tumor diameter was significantly reduced and the average survival time was increased with phytic acid. gamma-Oryzanol tended to decrease the size of the tumor but without significant difference. These results indicate that phytic acid inhibits hepatic and mammary carcinogenesis, while its Na-salt is a promoter of bladder carcinogenesis. The effect of phytic acid itself on urinary bladder carcinogenesis is equivocal. gamma-Oryzanol is a promoter of lung carcinogenesis but its effect is weak and exerted only at a very high dose level.
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PMID:Modifying effects of phytic acid and gamma-oryzanol on the promotion stage of rat carcinogenesis. 1062 36

Molecular analysis of malignant transformation in Barrett's epithelium provides insight into the temporal nature and significance of individual genetic events during multistep esophageal carcinogenesis. Potential targets for intervention in esophageal neoplasms include mutations involving retinoblastoma (Rb) and p53 tumor-suppressor pathways as well as tyrosine kinase cascades, which are known to promote cell cycle progression. Data from recent experiments provide the preclinical rationale for novel pharmacologic interventions in established esophageal cancers, and suggest strategies for chemoprevention in patients at risk for the development of these neoplasms.
Dis Esophagus 1999
PMID:Strategies for molecular intervention in esophageal cancers and their precursor lesions. 1063 9

Surgically induced duodenal reflux results in cancer development in the rat esophagus. One proposed mechanism of carcinogenesis relies on the production of carcinogens in the presence of bacterial overgrowth. Against this background, intestinal microflora in the rat jejunum was analyzed before and after reflux-inducing surgery. Total gastrectomy and esophagojejunostomy were performed on Sprague-Dawley rats to produce esophageal reflux of duodenal juice (n = 12). Three days before surgery they were randomized into three groups: animals which received tap water; animals which received acidified water at pH 1.8; and animals subjected to oral decontamination with triple antibiotics. During surgery and at autopsy after 2 weeks, intestinal juice was aspirated and analyzed immediately for bacterial content. The physiologic microflora of the rat jejunum contained Lactobacillus spp. and Bacteroides spp., both of which were resistant to the antibiotic regimen. Bacterial overgrowth with fecal bacteria was found following surgery. Acidified water did not alter the intestinal microflora. Triple antibiotics eliminated Escherichia coli and Proteus spp. and reduced the concentration of Enterococcus spp. Bacterial overgrowth by bacteria of the fecal flora occurs in the rat model of esophageal adenocarcinoma with the potential to catalyze the production of carcinogens.
Dis Esophagus 2000
PMID:Evaluation of the intestinal microflora in the rat model for esophageal adenocarcinoma. 1100 30

A report of radiation-induced squamous cell carcinoma in situ of the esophagus is presented. This report indicates that the patient developed the carcinoma in situ many years after chest wall irradiation for breast cancer treatment. A review of the literature with respect to carcinogenesis after radiotherapy is included and recommendations for the follow-up of patients having mediastinal radiation are suggested.
Dis Esophagus 2000
PMID:Radiation-induced esophageal squamous cell carcinoma in situ. 1120 45


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