Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A bioassay of technical-grade picloram for possible carcinogenicity was conducted by administering the test chemical in feed to Osborne-Mendel rats and B6C3F1 mice. Groups of 50 rats and 50 mice of each sex were administered picloram in the diet at one of the following doses for 80 weeks. Time-weighted average doses for the rats were 7,437 or 14,875 ppm; those for the mice were 2,531 or 5,062 ppm. The rats were then observed for 33 weeks, the mice for 10 weeks. Matched controls consisted of groups of 10 untreated rats or 10 untreated mice of each sex; pooled controls, used for statistical evaluation, consisted of the matched control groups combined with 33 untreated male and 30 untreated female rats or mice from similar bioassays of three other test chemicals. All surviving rats were killed at 113 weeks; all surviving mice were killed at 90 weeks. Survival was adequate for meaningful statistical analyses of the incidences of tumors in rats and mice of both sexes. Mean body weights of the high-dose rats were lower than those of matched controls during the first part of the study; however, beginning at approximately 80 weeks, mean weights of controls were lower than those of treated animals. Body weights of the mice were unaffected by the picloram. In rats, a relatively high incidence of follicular hyperplasia, C-cell hyperplasia, and C-cell adenoma of the thyroid occurred in both sexes. However, the statistical tests for adenoma did not show sufficient evidence for association of the tumor with picloram administration. An increased incidence of hepatic neoplastic nodules was observed in treated male and female rats as compared with untreated animals. This lesion is considered to be a benign tumor. In male rats the lesion appeared only in three animals of the low-dose treatment group and was not significant when compared with the controls; however, the test for positive dose-related trend in females was significant (pooled controls 0/39, low-dose 5/50, high-dose 7/49, P=0.016) and the incidence in the high-dose group was significant (P=0.014) when compared with that in the pooled-control group. There was also one hepatocellular carcinoma in a low-dose male rat and one in a high-dose female rat. In both males and females, there was a possibly treatment-related lesion of the liver diagnosed as foci of cellular alteration. The incidences of this latter lesion were, female rats: matched controls 1/10, low-dose 8/50, high-dose 18/49; male rats: matched controls 0/10, low-dose 12/49, high-dose 5/49. Thus, there is evidence that picloram affected the livers of rats of both sexes, but more particularly those of the females. No tumors were found in male or female mice or male rats at incidences that could be significantly associated with treatment, and it is concluded that picloram was not carcinogenic for B6C3F1 mice or male Osborne-Mendel rats. In female rats, however, the incidence of neoplastic nodules of the liver, benign tumors, was associated with treatment with picloram. It is concluded that under the conditions of the bioassay, the findings are suggestive of the ability of the compound to induce benign tumors in the livers of female Osborne-Mendel rats.
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PMID:Bioassay of picloram for possible carcinogenicity. 1284 85

Bioassays of technical-grade aldrin and dieldrin for possible carcinogenicity were conducted by administering the test materials in feed to Osborne-Mendel rats and B6C3F1 mice. Aldrin Groups of 50 rats of each sex were administered aldrin at one of two doses, either 30 or 60 ppm. Male rats were treated for 74 weeks, followed by 37-38 weeks of observation; female rats were treated for 80 weeks, followed by 32-33 weeks of observation. Matched controls consisted of groups of 10 untreated rats of each sex; pooled controls, used for statistical evaluation, consisted of the matched-control groups combined with 58 untreated males and 60 untreated females from similar bioassays of other chemicals. All surviving rats were killed at 111-113 weeks. Groups of 50 mice of each sex were administered aldrin at one of two doses for 80 weeks, then observed for 10-13 weeks. Time-weighted average doses were 4 or 8 ppm for males and 3 or 6 ppm for females. Matched controls consisted of groups of 20 untreated male mice and 10 female mice; pooled controls, used for statistical evaluation, consisted of the matched-control groups combined with 92 untreated male and 79 untreated female mice from similar bioassays of other chemicals. All surviving mice were killed at 90-93 weeks. Mean body weights attained by the rats and mice fed diets containing aldrin were similar to those of the controls during the first year of the study; however, mean body weights of the treated rats were lower than those of the controls during the second year of the study. Hyperexcitability was observed in all treated groups with increasing frequency and severity during the second year. Aldrin produced no significant effect on the mortality of rats or of male mice, but there was a dose-related trend in the mortality of female mice, primarily due to the early deaths in the high-dose groups. There was an increased combined incidence of follicular-cell adenoma and carcinoma of the thyroid both in male rats fed aldrin (matched controls 3/7, pooled controls 4/48, low-dose 14/38, high-dose 8/38) and female rats fed aldrin (matched controls 1/9, pooled controls 3/52, low-dose 10/39, high-dose 7/46). These incidences were significant in the low-dose but not in the high-dose groups both of males (P=0.001) and females (P=0.009) when compared with the pooled controls. Comparisons with matched controls, however, were not significant. Cortical adenoma of the adrenal gland was also observed in aldrin-treated rats in significant proportions (P=0.001) in low-dose (8/45) but not in high-dose (1/48) females when compared with pooled controls (0/55). Because these increased incidences were not consistently significant when compared with matched rather than pooled control groups, it is questionable whether the incidences of any of these adrenal tumors were associated with treatment. In male mice, there was a significant dose-related increase in the incidence of hepatocellular carcinomas (matched controls 3/20, pooled controls 17/92, low-dose 16/49, high-dose 25/45) when compared with either matched controls (P=0.001), or pooled controls (P<0.001). The incidence in the high-dose group was significant when compared with matched controls (P=0.002) or pooled controls (P<0.001). Dieldrin Groups of 50 rats and 50 mice of each sex were administered dieldrin at one of two doses. Low-dose rats and both low-and high-dose mice were treated for 80 weeks, followed by observation periods of 30-31 weeks for rats and 10-13 weeks for mice. Treatment of high-dose rats was terminated after 59 weeks and followed by 51-52 weeks of observation. Time-weighted average doses doses for rats were 29 or 65 ppm; doses for mice were 2.5 or 5 ppm. Matched controls consisted of groups of 10 untreated rats of each sex and 20 untreated male mice and 10 female mice; pooled controls, used for statistical evaluation, consisted of the matched-control groups combined with untreated animals from similar bioassays of other chemicals (58 male and 60 female rats, 92 male and 79 female mice). All surviving rats were killed at 110-111 weeks, and all surviving mice at 90-93 weeks. Mean body weights attained by the rats and mice fed diets containing dieldrin showed little or no differences compared with those of the controls during the first year of the study; however, mean body weights of the treated rats were lower than those of the controls during the second year of the study. Hyperexcitability was observed in all treated groups with increasing frequency during the second year, especially in high-dose rats. There was a marked increase in the mortality rate of rats during the first 90 weeks of the study. However, because of the high rates of mortality in the control groups during the remaining 20 weeks, survival could not be shown to be statistically dose responsive. In rats, there was a significant (P=0.007) difference between the combined incidence of adrenal cortical adenoma or carcinoma in the low-dose females (6/45) and that in the pooled controls (0/55). Although this tumor was also found in animals treated with aldrin, it is not clearly associated with treatment, because the incidence in the high-dose (2/40) was not significant, and the incidences were not significant when matched, rather than pooled, controls were used for comparison. In male mice, there was a significant positive dose-related trend (P=0.020) in the incidence of hepatocellular carcinomas using the pooled controls (pooled controls 17/92, low-dose 12/50, high-dose 16/45). When high-dose males were compared with the pooled controls, the results were also significant (P=0.025). It is concluded that under the conditions of these bioassays, none of the tumors occurring in Osborne-Mendel rats treated with aldrin or dieldrin could clearly be associated treatment. Aldrin was carcinogenic for the liver of male B6C3F1 mice producing hepatocellular carcinomas. With dieldrin, there was a significant increase in the incidence of hepatocellular carcinomas in the high-dose males which may be associated with treatment.
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PMID:Bioassays of aldrin and dieldrin for possible carcinogenicity. 1284 87

A bioassay of technical-grade captan for possible carcinogenicity was conducted by administering the test material in feed to Osborne-Mendel rats and B6C3F1 mice. Groups of 50 rats of each sex were administered one of two doses of captan for 80 weeks, then observed for 33 or 34 weeks. The time-weighted average doses for both sexes of rats were 2,525 or 6,050 ppm. Matched controls consisted of groups of 10 untreated rats of each sex; pooled controls, used for statistical evaluation, consisted of the matched controls combined with 75 untreated male and 75 untreated female rats from similar bioassays of six other test chemicals. All surviving rats were killed at 113-114 weeks. Groups of 50 mice of each sex were administered the test material at one of two doses, either 8,000 or 16,000 ppm, for 80 weeks, then observed for 11 weeks. Matched controls consisted of groups of 10 untreated mice of each sex; pooled controls, used for statistical evaluation, consisted of the matched controls combined with 80 untreated male and 80 untreated female mice from similar bioassays of six other test chemicals. All surviving mice were killed at 90-91 weeks. The mean body weights of both low- and high-dose rats and high-dose mice were lower than those of the matched controls throughout most of the study. Mortality rates did not show statistically significant dose-related trends in either sex of either species. In rats, a positive dose-related trend and a difference between incidences of tumors in high-dose and pooled-control groups were found in females when the data for adrenal cortical adenoma were combined with those for adrenal cortical carcinoma (pooled controls, 0/64, low-dose 2/50, high-dose 3/47, P=0.047). There was also a positive dose-related trend for the incidence of C-cell adenoma of the thyroid in female rats (pooled controls 1/66, low-dose 1/49, high-dose 4/44, P=0.035). These endocrine tumors in female rats are believed to have been spontaneous, and not related to treatment. In mice, the incidences of polypoid carcinoma (adenocarcinoma in adenomatous polyp) of the duodenum were statistically significant using tests for a positive dose-related trend both in male mice (pooled controls 0/68, low-dose 1/43, high-dose 3/46, P=0.033) and in female mice (pooled controls 0/68, low-dose 0/49, high-dose 3/48, P=0.022). When the incidences of adenomatous polyp, NOS (not otherwise specified), were combined with those of polypoid carcinoma for statistical analysis, the tests for male mice indicated a substantial increase in significance (pooled controls 0/68, low-dose 3/43, high-dose 5/46, P=0.008). It is concluded that under the conditions of this bioassay, tumors in the duodenum of B6C3F1 mice were associated with treatment with captan, but there was no convincing evidence that the tumors observed in Osborne-Mendel rats were related to treatment.
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PMID:Bioassay of captan for possible carcinogenicity. 1285 54


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