¿Existe alguna relación entre la adicción a drogas y el desarrollo de un carcinoma de células en anillo de sello gástrico? / No disponible

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Tumor induction by azoxymethane (AOM) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in F344 rat gastric mucosa featuring intestinal metaplasia caused by X-irradiation.

Male F344 5-week-old rats were X-irradiated, and 16 weeks after the first dose, azoxymethane (AOM) was injected or 2-amino-1 -methyl-6-phenylimidazo [4,5-b]pyridine (PhIP) was given by intragastric intubation. Tumors in the pylorus of the glandular stomach were observed in 4 out of the 29 animals receiving X-rays + AOM and in 4 out of the 25 animals receiving X-rays + PhIP, 12 months after administration. No such lesions were found in the chemical or X-ray alone groups. Intestinal metaplasia and some induced tumors were positive for CDX2. It was concluded that the presence of intestinal metaplasia may increase sensitivity to the induction of gastric tumors by colon carcinogens.

Eradication diminishes enhancing effects of Helicobacter pylori infection on glandular stomach carcinogenesis in Mongolian gerbils.

To investigate the nature of the link between Helicobacter pylori (Hp) infection and stomach carcinogenesis, a study of the glandular stomach of Mongolian gerbils (MGs) was performed. MGs were treated with N-methyl-N-nitrosourea (MNU), followed by inoculation with Hp (groups 1 and 2) or without Hp (group 3), or infected with Hp (groups 4 and 5) or inoculation without Hp (group 6) followed by MNU administration. At week 21, the animals in groups 2 and 5 underwent an eradication procedure. At week 50, the incidences of adenocarcinomas in group 1 (15 of 23) and group 4 (9 of 26) were significantly higher than in group 3 (1 of 15) and group 6 (1 of 18), respectively. Moreover, those in group 2 (5 of 24) and group 5 (2 of 22) were lower than in groups 1 and 4, respectively. This study shows that Hp eradication may be useful as a prevention approach against stomach cancer.

Azoxymethane-induced aberrant crypt foci and colorectal tumors in F344 rats: sequential analysis of growth.

Previous studies are consistent with the hypothesis that aberrant crypt foci (ACF) could be intermediate biomarkers in colorectal carcinogenesis. The present controlled experimental trial was performed to sequentially analyze ACF progression in rat colonic mucosa. F344 rats were administered 2-weekly doses of azoxymethane (15 mg/kg body weight, s.c.) and sacrificed 6, 12, 20, 30 and 36 weeks after the first carcinogen injection. Control groups of untreated rats were sacrificed at the same time points. The number of ACF per area, their multiplicity (number of crypts per focus), ACF frequency and multiplicity according to each colonic site, histology of ACF and macroscopic lesions were recorded. No ACF were found in control animals. In treated animals, the number of ACF per area and the multiplicity progressively and significantly increased throughout the study. ACF were prevalent in the mid colon. Lower frequencies were registered in the distal colon and rectum. ACF were rare in the proximal colon and cecum. By histology, ACF presented superficial and extensive hyperplasia. Tumors were found in the 30th and 36th week. Adenomas and well-differentiated adenocarcinomas were in the distal colon. All proximal neoplasms were signet ring cell carcinomas. In our study, ACF growing features and distribution are not correlated to adenoma and adenocarcinoma distribution. It is conceivable that signet ring cell carcinomas arising in the proximal colon, where ACF are rare, could present a different pathway of growth. The preneoplastic role of ACF and their function as intermediate biomarkers in colorectal carcinogenesis remain to be clarified.

Helicobacter pylori infection enhances N-methyl-N-nitrosourea-induced stomach carcinogenesis in the Mongolian gerbil.

No previous report has demonstrated the relationship between Helicobacter pylori (HP) infection and gastric carcinogenesis in an experimental animal model. A total of 170 male Mongolian gerbils (MGs) were divided into nine groups (18 < or = n < or = 20 for each group). MGs of four groups were inoculated with HP before or after continuous N-methyl-N-nitrosourea (MNU) administration via the drinking water. Both intestinal-type and diffuse-type adenocarcinomas, including signet ring-cell carcinomas, were found at 40 weeks after the study commenced, but only in the HP inoculation groups with MNU exposure and not in the MNU alone or HP inoculation alone control groups. The present findings demonstrate that HP infection increases the incidence of MNU-induced adenocarcinoma of the glandular stomach in MGs.

Effects of apple pectin on fecal bacterial enzymes in azoxymethane-induced rat colon carcinogenesis.

Because of the potential significance of colonic bacteria in colon carcinogenesis, we investigated the effect of pectin of different types on fecal bacterial enzymes (beta-glucuronidase, beta-glucosidase and tryptophanase) at various periods of time after feeding rats with pectin-containing diets during azoxymethane-induced colon carcinogenesis. The diet supplemented with 20% apple pectin or 20% citrus pectin decreased the multiplicity of colon tumors, and the number of tumors was significantly decreased in the group fed apple pectin. The incidence of colon tumors in the apple pectin group was lower than that in the control group. The mean tumor size was similar among the three groups. Apple pectin feeding decreased fecal beta-glucosidase and tryptophanase levels. Furthermore, a significant decrease in the activity of beta-glucuronidase was observed in the apple pectin group during the initiation phase. These findings suggest that the protective effect of pectin on colon carcinogenesis may be dependent on the type of pectin and be related to the decrease of beta-glucuronidase activity in the initiation stage of carcinogenesis.

Induction of glandular stomach cancers in C3H mice treated with N-methyl-N-nitrosourea in the drinking water.

Establishment of an animal model of stomach carcinogenesis in mice was attempted using N-methyl-N-nitrosourea (MNU) in the drinking water. One hundred and forty-eight male 6-week-old C3H mice were given MNU in their drinking water at a concentration of 120 ppm (group 1), 60 ppm (group 2), 30 ppm (group 3) or 0 ppm (group 4) for 30 weeks. At the end of this time, dose-related induction of adenomatous hyperplasias was found. From weeks 31 to 54 adenocarcinomas developed in a dose-dependent manner in groups 1, 2 and 3. In total, 6 well differentiated and 5 poorly differentiated adenocarcinomas as well as 6 signet ring cell carcinomas arose in 15 stomach cancer-bearing animals in group 1, 4 well differentiated and 2 poorly differentiated adenocarcinomas with one signet ring cell carcinoma in 5 mice of group 2 and one well differentiated adenocarcinoma in group 3. In the forestomach, only one squamous cell carcinoma was found at week 54 in group 1 along with a single well differentiated adenocarcinoma in the duodenum. Thus, MNU in the drinking water selectively induced neoplastic lesions in the glandular stomach epithelium of mice.