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At least 829 records · Page 46Linked to original sources
PubMed1987

Bromodichloromethane, a trihalomethane that produces neoplasms in rodents.

Bromodichloromethane, a trihalomethane found in water supplies after chlorination, was administered by gavage in corn oil to male and female F344/N rats and B6C3F1 mice for up to 2 years at dose levels of 0, 50, or 100 mg/kg to rats, 0, 25, or 50 mg/kg to male mice, and 0, 75, or 150 mg/kg to female mice. Survival at 2 years in rats and in male mice was comparable among groups and was greater than 50% at the termination of the experiment. Survival in female mice was greater than 50% in all groups until week 84 but was reduced toward the end of the study because of ovarian abscesses in some female mice. There was clear evidence of carcinogenicity in males and females of both species as shown by increased incidences of tubular cell adenomas and adenocarcinomas in the kidney and adenocarcinomas and adenomatous polyps in the large intestine in male and female rats, increased incidences of tubular cell adenomas and adenocarcinomas in the kidney of male mice, and increased incidences of hepatocellular adenomas and carcinomas in female mice. Of the three trihalomethanes studied to date in the National Cancer Institute/National Toxicology Program (chloroform, chlorodibromomethane, or bromodichloromethane) bromodichloromethane caused the widest spectrum of neoplasms in rodents.

Adenocarcinoma↗
PubMed1986

[Radiological differential diagnosis of colorectal cancer].

This study was undertaken to evaluate the radiological diagnosis of colorectal polypoid lesions between 0.6 cm and 3.0 cm in size. Lesions less than 0.6 cm were mostly benign or, on rare occasions, early carcinomas limited to the mucosa. Lesions more than 3.0 cm in size were mostly advanced carcinomas. Lesions were classified by modified Maruyama's classifications as follows, type "a" (lesion with long stalk), type "b" (lesion with short or sessile lesion), type "c" (plaque-like lesion), type "d" (lesion with central depression) and type "e" (the others). Type "a" lesions were either benign or early cancers but these could not be distinguished radiologically. Type "b" and "c" lesions more than 1.0 cm in size and with indentation of colonic wall, had a great probability of being early cancer. Type "d" lesions with a slight depression were either benign or early cancers but type "d" lesion with a moderate depression were all advanced cancers. Type "e" lesions were mostly villous tumors so that it was difficult to diagnose whether these were cancer or not.

Adenocarcinoma↗
PubMed1994

Progression toward malignancy of hamartomas in a patient with Peutz-Jeghers syndrome: case report and literature review.

Peutz-Jeghers syndrome, inherited in an autosomal dominant fashion, is characterized by hamartomatous polyps of the gastrointestinal tract and by mucocutaneous pigmentation. The frequency of gastrointestinal malignant disease in this syndrome is estimated to be 2% to 3%. The authors review reports associating Peutz-Jeghers syndrome with malignant disease and present a patient who had advanced jejunal adenocarcinoma in association with Peutz-Jeghers syndrome. It has not been determined with certainty whether the malignant lesions arise from hamartomas, from associated adenomatous polyps or from the normal mucosa. Histologic examination of the excised specimen from the patient reported in this paper showed areas typical of a hamartoma as well as areas of hyperplasia, adenoma with mild to severe dysplasia and carcinoma in situ all in the same polyp. These findings suggest that the hamartomatous polyps found in Peutz-Jeghers syndrome have the potential to undergo malignant transformation.

Adenocarcinoma, Mucinous↗
PubMed1989

High-grade non-Hodgkin's lymphoma complicating polypoid nodular lymphoid hyperplasia and multiple lymphomatous polyposis of the intestine.

Three patients with multiple lymphoid polyps of the small intestine--two with nodular lymphoid hyperplasia and one with multiple lymphomatous polyposis--developed high-grade B-cell lymphomas. A literature search has revealed only 10 previous cases of nodular lymphoid hyperplasia complicated by lymphoma and none of an association between multiple lymphomatous polyposis and high-grade lymphoma.

Adult↗
PubMed2004

Analysis of reciprocal congenic lines reveals the C3H/HeJ genome to be highly resistant to ApcMin intestinal tumorigenesis.

Genetic background affects polyp development in the Multiple intestinal neoplasia (Apc(Min)) mouse model. The Modifier of Min 1 (Mom1) locus accounts for approximately 50% of the variation in polyp multiplicity. We generated reciprocal congenic lines, such that the recipient C57BL/6J (B6) strain carries a donor C3H/HeJ (C3H) Mom1 allele, and the recipient C3H strain carries a donor B6 Mom1 allele. Hybrid progeny from congenic females mated to B6 Apc(Min/+) males were analyzed. A single C3H Mom1 locus on the B6 background reduced small intestinal polyp numbers by 50% and colon polyp incidence by 66% compared to their susceptible B6 Mom1(S/S)Apc(Min/+) siblings. These findings show that the C3H genome contains a resistant Mom1(R) locus. The reciprocal congenic line, which carries the susceptible B6 Mom1(S) locus on the C3H background, reduced small intestinal polyp numbers by 80% and colon polyp incidence by 95% compared to B6 Mom1(S/S)Apc(Min/+) mice. These data demonstrate that unidentified modifiers in the C3H strain can suppress intestinal polyp multiplicity in Apc(Min/+) mice, and act in the absence of a resistant Mom1(R) locus.

Adenomatous Polyposis Coli↗
PubMed1985

Prevalence of polyps in an autopsy series from areas with varying incidence of large-bowel cancer.

The results of this multicentre autopsy study emphasize the relationship between the prevalence of adenomas and the incidence of large-bowel cancer. The highest proportion of autopsies with adenomas was observed in the area with the highest incidence of large-bowel cancer. The segmental distribution of adenomas within the colon was found to be similar to the site distribution of cancer. However, the lowest proportion of adenomas was found in the rectum, the segment in which cancer is most frequent. The latter finding suggests that either the adenoma-carcinoma sequence is a less important pathway in the pathogenesis of rectal cancer, or that more rectal than colonic adenomas become malignant. The high proportion of hyperplastic polyps in the rectum, and statistically significant regional differences following the same patterns as the incidence of rectal cancer suggest that there could be at least an indirect relationship between hyperplastic polyps and cancer of the rectum. Adenomas of both colon and rectum were more frequent in men than in women, contrary to findings with colon cancer. However, as for colon cancer, the sex ratio of adenomas changed with age, from slightly below unity in persons under 65, to above unity for those aged 65 and over. A major difficulty that emerged was the histological identification of "polyps" because of the degree of autolysis of epithelial cells in the mucous membrane, and this difficulty largely contributed to the poor consistency of histological reporting. Regular consistency surveys of histological preparations should be recommended in any type of multicentre study in which histological examination is included.

Adult↗