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

This study was undertaken to determine if the construction of an ileal reservoir induces mucosal changes that can potentiate the effect of a chemical carcinogen (1,2-dimethylhydrazine) on ileal mucosa. Animals were divided into three groups: 1) sham operation (n = 19), 2) total colectomy with ileorectal anastomosis (n = 20), 3) total colectomy with an ileal reservoir made of terminal ileum sutured to the rectum (n = 20). An adaptation period of 12 weeks was allowed to promote fecal stasis and the histologic changes before exposure to weekly subcutaneous injections of DMH (25 mg/kg) for 16 weeks. Sodium butyrate was added to the diet as a tumor promotor. All animals were sacrificed one month later. Fecal stasis, along with enlargement, occurred in all the reservoirs (mean dimensions, 74 X 58 X 43 mm). Their mean volume was 88 +/- 14 ml. The histologic changes in the ileal reservoirs were: chronic inflammation (14/20), villous atrophy (14/20), and atrophy of the glands (8/20). In group 3, five carcinomas were seen. There were three in the duodenum and two in the reservoirs. In contrast, 21 carcinomas were detected in the control groups. There were 17 in the colon, 3 in the jejunum, and 1 in the ileum. No significant difference in the number of carcinomas was seen in the ileum with and without reservoir. Although it is possible to induce carcinomas in ileal reservoirs, the incidence remained significantly less than in the colon. In conclusion, the histologic changes induced by the construction of an ileal reservoir do not increase the risk of malignant transformation in the DMH model for intestinal carcinogenesis.
Dis Colon Rectum 1990 Jan
PMID:An assessment of the risk of neoplasia in long-term ileal reservoirs using the DMH rodent model. 229 74

The effects of age on multi-organ carcinogenesis induced by 3,2'-dimethyl-4-aminobiphenyl (DMAB) in male F344 rats were examined. Groups of 5-, 35-, and 65-week-old animals were given 4 weekly sc injections of DMAB at a dose of 200 or 150 mg/kg body weight. Prostate carcinomas were induced in 8 to 19% of rats treated, no significant differences in the incidence between different ages being observed. Tumors in the small intestine, skin, pancreas and peritoneum, however, developed more frequently in young than in old animals, whereas higher incidences of testis, preputial and mammary gland lesions were found in the 35- and/or 65-week-old groups. Colon and Zymbal gland carcinogenesis did not reveal any age dependence.
 ...
PMID:Effects of age on multiple organ carcinogenesis induced by 3,2'-dimethyl-4-aminobiphenyl in rats, with particular reference to the prostate. 250 Dec 47

To examine the carcinogenetic and growth inhibitory effects of OK-432, large-bowel carcinoma was induced experimentally in rats by intrarectal injection of N-methyl-N-nitrosourea (MNU), and OK-432 was administered intradermally. Rats were sacrificed after six months and the large intestine was cut into serial sections. Histopathologic examination and analysis of the infiltrating mononuclear cells, using monoclonal antibodies, were performed. The average rate of carcinogenesis per rat was 15.7 +/- 8.5 in the MNU alone group (n = 10) and 8.3 +/- 3.5 in the MNU and OK-432 group (n = 6). The invasion was deeper than the muscularis propria in 16 out of 157 lesions (10.2 percent) in the MNU alone group and in one out of 50 lesions in the MNU + OK-432 group (2.0 percent) (P less than 0.05). When time of appearance of atypical glands or carcinomas were compared in the MNU alone and MNU + OK-432 group, carcinogenesis was found to be delayed in the MNU + OK-432 group. In the investigation of infiltrating mononuclear cells using monoclonal antibodies, there were increases in helper T cells in both the MNU alone and MNU + OK-432 groups, but there was little difference between the two groups. The results of this study suggest that the suppression of experimental carcinogenesis in the large bowel by the concomitant administration of OK-432 with MNU, may be due to the enhanced activation or prolonged activated state of immunocompetent cells, which appear via antigen recognition, by OK-432.
Dis Colon Rectum 1989 Oct
PMID:Effect of OK-432 on large-bowel carcinogenesis in rats. 255 12

The epithelial expression of carbohydrate antigen, stage-specific embryonic antigen 1 (SSEA-1) was examined immunohistochemically in noncancerous specimens from patients with familial polyposis coli, and compared with the colorectal epithelia from patients with sporadic colorectal cancer. In mucosa remote from carcinoma of sporadic cases, SSEA-1 was expressed only faintly in the lower crypts. In mucosa adjacent to carcinoma of sporadic cases, SSEA-1 was expressed not only in the lower crypts but also in the upper crypts. These results corresponded to those observed in the authors' previous study. In the flat mucosa of familial polyposis coli cases, SSEA-1 was detected not only in the lower crypts, but also in both upper crypts and the surface epithelium in contrast with the flat mucosa of sporadic cases. The staining pattern in the upper crypts of the flat mucosa of familial polyposis coli cases was very similar to that of the mucosa adjacent to carcinoma of sporadic cases, but was stronger and more diffuse in the surface epithelium. In microscopic adenomas, SSEA-1 was expressed diffusely. These results demonstrate that the flat mucosa of patients with familial polyposis coli shows preneoplastic changes similar to those in the mucosa adjacent to carcinoma of sporadic cases, and that SSEA-1 is related to adenoma formation in the early stage of carcinogenesis in the colorectum. In addition, the results suggest that immunohistochemical studies of flat mucosa may be useful for the early detection of high-risk individuals in a familial polyposis coli family.
Dis Colon Rectum 1987 Jun
PMID:The expression of stage-specific embryonic antigen 1 in the noncancerous colorectal epithelia of familial polyposis coli. 288 60

The cancers consistently associated with ingestion of alcohol, the head and neck cancers, are also associated with tobacco use and arise from epithelia that are in direct contact with both agents. Tobacco smoking-related cancers at sites not directly in contact with alcoholic beverages, that is, lung, bladder, and perhaps pancreas, do not consistently show a relationship to alcohol consumption, although lung and pancreatic tumors are associated in some studies. Liver cancer was thought to be strongly related to alcohol consumption on epidemiological grounds and because of its relationship to cirrhosis. As knowledge of the viral etiology of some cirrhoses has evolved and as methods to detect viruses have developed, the significant association between hepatitis B virus and hepatocellular carcinoma has become clear. Alcohol and hepatitis B virus may interact in the etiology of the disease and have important separate roles as well. There are epidemiologic and experimental data showing that malnutrition (resulting from poor food choice), economic deprivation, or alcoholism contributes to the risk for head, neck, and liver cancers. Colon cancers occur about equally in men and women, are found in well-nourished populations, and are not associated with tobacco smoking. Rectal cancers show a preponderance of cases in men but are frequently found in women as well and are not thought to be associated with smoking or malnutrition. The association between colorectal cancers and alcohol consumption, when it is found, apparently occurs at even relatively low alcohol intakes and is often stronger for consumption of beer than of other beverages. Nutritional and metabolic mechanisms proposed for the influence of alcohol on carcinogenesis are supported by studies in human subjects and laboratory animals. Animal models are needed in which effects of ethanol on carcinogenesis can be consistently demonstrated and which can then be used to examine mechanisms.
 ...
PMID:Alcohol and cancer. 303 1

The effect of various levels of dietary Menhaden fish oil containing omega-3 fatty acids plus corn oil containing omega-6 fatty acids fed during the postinitiation phase of colon carcinogenesis was studied in male F344 rats. Starting at 5 weeks of age, groups of animals were fed the 5% corn oil (5% CO) diet. At 7 weeks of age, all animals except the vehicle-treated controls were administered s.c. injections of azoxymethane (15 mg/kg body wt/week for 2 weeks). 4 days after carcinogen or vehicle treatment, groups of animals were transferred to experimental diets containing 4% Menhaden oil + 1% corn oil (4% MO + 1% CO), 23.5% corn oil (23.5% CO), 17.6% corn oil + 5.9% Menhaden oil (17.6% CO + 5.9% MO), 11.8% corn oil + 11.8% Menhaden oil (11.8% CO + 11.8% MO), or 5.9% corn oil + 17.6% Menhaden oil (5.9% CO + 17.6% MO) and fed these diets until termination of the experiment at Week 38 after carcinogen treatment. An additional group consuming a 5% CO diet was continued on these diets. Colon mucosal ornithine decarboxylase activity and microsomal fatty acid composition of colon mucosa were measured in vehicle-treated animals fed experimental diets for 14 weeks. Fatty acids were also analyzed in the microsomal fraction of colon tumors at termination of the experiment. The body weights of animals fed various experimental diets were comparable. Feeding of high fat diets containing 17.6% CO + 5.9% MO, 11.8% CO + 11.8% MO, or 5.9% CO + 17.6% MO significantly inhibited the incidence (percentage of animals with tumors) of colon adenocarcinomas compared to that of 23.5% CO diet. However, the multiplicity (number of tumors/rat) of colon adenocarcinomas was significantly inhibited only in groups fed the 5.9% CO + 17.6% MO compared to those fed the 23.5% CO diet. The incidence and multiplicity of adenocarcinomas were greater in animals fed the 23.5% CO diet compared to those fed the 5% CO diet. Colonic mucosal ornithine decarboxylase activity was lower in animals fed the 11.8% CO + 11.8% MO, 5.9% CO + 17.6% MO, 5% CO, and 4% MO + 1% CO diets compared to the levels in animals fed the 23.5% CO diet. The increasing levels of Menhaden oil in the diet significantly increased the omega-3 fatty acids such as eicosapentaenoic acid and docosahexaenoic acid and decreased the omega-6 fatty acids such as linoleic acid, linolenic acid, and arachidonic acid in microsomal fractions from colonic mucosa and tumors.
 ...
PMID:Effect of different levels of omega-3 and omega-6 fatty acids on azoxymethane-induced colon carcinogenesis in F344 rats. 318 73

Serum concentration of gastrin determined by radioimmunoassay in 90 consecutive patients who underwent colonoscopy, and serum levels of gastrin in patients with colorectal neoplasia and controls were compared. Based on clinical history, findings of colonoscopy, and pathologic examinations of biopsies, 80 patients were considered eligible for the study. Serum levels of gastrin in 36 controls were 54.1 +/- 13.1 pg/ml and did not differ from serum levels of gastrin in 44 patients with colorectal neoplasia. There was also no significant difference in serum levels of gastrin among 28 patients with adenomas and 16 patients with carcinoma. The present study disclosed that carcinogenesis of the colon and rectum was not associated with hypergastrinemia.
Dis Colon Rectum 1988 Sep
PMID:Serum levels of gastrin in patients with colorectal neoplasia. 271 39

From the time of Hippocrates until the late 19th century, physicians and surgeons were convinced that surgical attempts at treating colorectal cancers were doomed to failure. This opinion stemmed from prevailing views on carcinogenesis. The three dominant theories, the humoral, mineral, and lymph theories, held that all cancers developed in tissue that had a diseased disposition. Thus, excision of the gross tumor mass alone seemed unlikely to cure the patient. Consequently, surgical treatment of all cancers, and in particular colorectal cancer, was vehemently condemned. The 19th century represented a transition period. Advances in surgical technique made excision of rectal cancers feasible. Unfortunately, classical views that resection of cancer was futile delayed the development of surgical treatment for colorectal cancer. Indeed, it was not until the late 19th century that a few individuals ignored these tenets of classical medicine and attempted local resections of rectal cancers. By the second quarter of the 20th century, a radical change occurred in the prevailing theories of carcinogenesis. Wide acceptance of the unicellular origin of cancer and the mucosal origin of colorectal cancers washed away admonitions against surgical treatment of colorectal cancers. It became axiomatic that all cancers, including colorectal cancers, could be cured surgically if treated while still local diseases.
Dis Colon Rectum 1988 Jul
PMID:Theories of carcinogenesis and their impact on surgical treatment of colorectal cancer. A historical review. 329 61

Life-long bowel habits of 685 colorectal cancer cases and 723 age/sex frequency matched community controls were investigated as one part of a large, comprehensive, population-based study of colorectal cancer incidence, etiology, and survival, The Melbourne Colorectal Cancer Study. Self-reported chronic constipation was statistically significantly more common in cases than in controls (P = .05). Three or more bowel actions per day were reported by more cases than controls but the total number of respondents in this subset consisted of only ten cases and two controls. Otherwise, the frequency and consistency of bowel motions was similarly distributed among cases and controls. Constipation disappeared as a significant risk when simultaneously adjusted for previously determined dietary risk factors, indicating that it is the diet and not the constipation that is associated with the risk of large-bowel cancer. Additionally, a highly statistically significant association (P = .02) was found with the risk of colorectal cancer in those who reported constipation and also had a high fat intake, a finding consistent with current hypotheses of colorectal carcinogenesis. It is concluded that chronic constipation, diarrhea, and the frequency and consistency of bowel motions, as well as laxative use, are unlikely to be etiologic factors in the development of colorectal cancer. Self-reported chronic constipation is a marginally significant indicator of excess risk of large-bowel cancer and may be used as one of the indices in the screening of individuals for this cancer.
Dis Colon Rectum 1988 Jul
PMID:The role of chronic constipation, diarrhea, and laxative use in the etiology of large-bowel cancer. Data from the Melbourne Colorectal Cancer Study. 339 Oct 59

Although no absolute certainty exists about the role of nutrition in the etiology of cancer, many facts in favor of the relationship became available during the last decades. Correlation studies, experimental work and to a lesser extent case-control studies made it possible to clarify the role of certain nutrients and foods in carcinogenesis. The most important cancer sites where nutrition could play a role are esophagus, stomach, colon, rectum, prostate and breast. Esophageal cancer is of a very complex etiology, in which alcohol intake plays an important role, at least in western countries. The cancer-promoting properties of alcohol intake are enhanced by smoking. Three factors from nutrition are probably related to stomach cancer, namely salt, nitrate/nitrite and vitamin C. Salt is caustic to the stomach mucosa, resulting in atrophic gastritis. Salt is also co-carcinogenic and stomach cancer-promoting in experimental animals. Nitrate is probably important at the stage of atrophic gastritis, where bacterial overgrowth, due to the high pH, converts nitrates in nitrites, making the loco synthesis possible of potent nitrosocarcinogens. Vitamin C inhibits the latter step. The epidemiological evidence for the role of those factors is provided. The most important among them is the strong and consistent association of stomach cancer mortality with stroke. Rectum, colon, prostate and breast cancer are related in some way to fat intake. They all seem positively related to saturated fat intake, whereas breast cancer is probably also promoted by polyunsaturated fat intake. However, polyunsaturated fat seems to be without effect on rectum cancer. Colon and prostate cancer are probably also influenced by polyunsaturated fat but to a lesser degree than breast cancer. An important argument for this are the positive ecological correlations between changes in rectum, colon and breast cancer mortality from 1968 on, and changes occurring in coronary heart diseases, stroke and diabetes mortality. Those six types of mortality are decreasing, or only slightly increasing in the USA, Belgium, France, the Netherlands, etc. They are strongly increasing in East European countries. The intake of saturated fat has generally decreased in the first group of countries, and has markedly increased in the second group.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Nutrition and cancer. 353 16


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>