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

The effect of reovirus type 3 infection on the pulmonary adenoma response to urethan in strain A mice was examined. Urethan carcinogenesis in this system was suppressed from 30 to 60% when mice were exposed to reovirus either 6 days before, on the same day as, or 14 days after urethan administration. These findings suggested that reovirus infection interfered with the progression of urethan-induced pulmonary adenoma rather than the induction of lung tumors by urethan. When mice received multiple exposures to reovirus, the lung tumor response was enhanced. These findings indicated that reovirus infection in particular and virus infection in general may play an important role in the carcinogenic response to environmental chemicals.
 ...
PMID:Effect of reovirus infection on pulmonary tumor response to urethan in strain A mice. 20 99

Sister-chromatid exchange (SCE) induction and cell cycle kinetics alterations by ethyl carbamate in bone marrow of non-gravid murine Swiss Webster, ICR/Jcl, and C57Bl/6J dams were evaluated, and data from non-gravid females were compared with those previously reported for pregnant dams of the same strains. In addition, lung adenoma induction by ethyl carbamate in gravid Swiss Webster dams, their offspring, and in non-pregnant Swiss Webster females was also determined. Relative cytogenetic and tumor responses in non-gravid and gravid Swiss Webster females and their offspring were compared. In contrast to the increased sensitivity reported for gravid Swiss Webster dams versus ICR/Jcl and C57Bl/6J dams, SCE responses to 1.1, 2.2, or 3.3 mmol/kg of ethyl carbamate in non-gravid females were approximately equivalent among strains. In Swiss Webster and C57Bl/6J (but not ICR/Jcl) strains, SCE responses in non-gravid females at 2.2 and 3.3 were significantly lower than those of their pregnant counterparts. Tumor induction by 3.3 mmol/kg ethyl carbamate paralleled relative SCE induction with Swiss Webster dams, demonstrating a 5-fold increase in the number of tumors relative to their offspring and a 4-fold enhancement of tumor induction relative to their non-pregnant counterparts.
 ...
PMID:Tumor formation and sister chromatid exchange induction by ethyl carbamate: relationships among non-pregnant murine females, gravid dams, and transplacentally exposed offspring. 136 58

Male CD-1 mice were exposed to a commercial formulation of 2,4-dichlorophenoxyacetic acid (2,4-D), the amine derivative, in the drinking water at concentrations ranging from 0 to 0.163% of the formulated product, equivalent to approximately 0-50 mg kg-1 day-1 2,4-D content. The effect of 2,4-D on urethan-induced pulmonary adenoma formation was evaluated following a 105-day exposure. Urethan-induced sleeping times observed following an i.p. injection of urethan (1.5 mg g-1) after 3 weeks of 2,4-D exposure were not altered by 2,4-D, indicating that 2,4-D did not influence urethan elimination. Pulmonary adenoma production, which was evaluated 84 days after urethan injection, was enhanced by 2,4-D exposure but had no effect on tumor size. The effect of 2,4-D on the incidence of spontaneous murine lymphocytic leukemia was evaluated during the 365-day treatment period. Mortality associated with the leukemia virus was not altered by 2,4-D treatment. Exposure to this commercial 2,4-D product at moderately high levels of exposure may modify the development or expression of certain tumors in CD-1 mice. The mechanism of the co-carcinogenic or tumor-promoting activity associated with 2,4-D exposure remains to be determined.
 ...
PMID:The effect of a commercial 2,4-D formulation on chemical- and viral-induced tumor production in mice. 143 Jul 74

Urethane-induced, lung adenoma multiplicity and histologic type vary among mouse strains. We asked whether the Pas genes which control multiplicity also determine adenoma structure. Lung adenomas from inbred mice, F1 hybrids, and recombinant inbred mice were classified by growth pattern as either solid or papillary. Since no correlation was observed between adenoma multiplicity and histologic type, no linkage apparently exists between the Pas genes and adenoma morphology. We propose the name Pah (Pulmonary Adenoma Histologic type) for the genes controlling lung adenoma growth patterns. Genetic analysis indicated dominance of the papillary phenotype, and that two or more Pah genes determine adenoma structure.
 ...
PMID:Lung adenoma structure among inbred strains of mice: the pulmonary adenoma histologic type (Pah) genes. 176 94

Female CD-1 mice were exposed to Tordon 202c, a herbicide containing 2,4-dichlorophenoxyacetic acid and picloram, in the drinking water for 15 w at concentrations ranging from 0 to 0.3% of the product formulation. After 3 w of the 15-w treatment period, the mice received 1.5 mg/g urethan ip. Pulmonary adenoma production was evaluated 12 w later. Tordon 202c exposure produced a dose-dependent increase in tumor number, but had no effect on tumor size. Urethan-induced sleeping times which reflected the rate of urethan metabolism or excretion were altered, but a specific dose-related effect which could be correlated with tumor production was not observed. This suggests that Tordon 202c exposure influences adenoma formation by immunological mechanisms rather than by causing indirect effects on urethan metabolism or excretion.
 ...
PMID:The effects of Tordon 202c exposure on urethan-induced lung adenoma formation in female CD-1 mice. 185 96

Murine susceptibility to ethyl carbamate-induced carcinogenesis is strain dependent. In vivo sister chromatid exchange (SCE) responses to ethyl carbamate were evaluated in bone marrow cells of gravid adenoma-susceptible (ICR/Jcl), and resistant (C57Bl/6J) and (DBA/2J) murine dams, as well as in liver cells of their respective ICR/Jcl, C57Bl/6J X DBA/2J (BDF1), and DBA/2J X C57Bl/6J (BDF), fetuses following a single intravenous injection of 1.1, 2.2, or 3.3 mmol/kg of ethyl carbamate on gestation day 13/14. Bone marrow tissues of C57Bl/6J and DBA/2J, but not ICR/Jcl dams, demonstrated greater sensitivity to SCE induction than liver cells of their respective fetuses. Furthermore, relative SCE responses in bone marrow among dams indicated greater sensitivity of the more tumor-susceptible ICR/Jcl and C57Bl/6J strains to SCE induction by ethyl carbamate relative to the more tumor-resistant DBA/2J strain. In addition, concurrent alterations (stimulation or inhibition) of bone marrow cell cycle kinetics by ethyl carbamate were consistent with hormone-related, strain-dependent hematopoietic stress during pregnancy.
 ...
PMID:Comparative in vivo sister chromatid exchange induction by ethyl carbamate in maternal and fetal tissues of tumor-susceptible and -resistant murine strains. 197 64

This study was designed to test the pulmonary tumor response to intratracheally instilled silica in Strain A mice. Urethane was used as a positive control. Silica treatment was utilized to evaluate the effect of a potent fibrinogen on pulmonary adenoma formation in this unique animal model. Urethane produced an increase in pulmonary tumor response in this study in agreement with previous investigations. Also, the background incidence of adenomas was comparable to other studies. Silica treatment did not affect tumor incidence either in terms of percent of mice with adenomas or average number of adenomas per mouse.
 ...
PMID:Pulmonary adenomas in A/J mice treated with silica. 216

Female Swiss mice were exposed to cadmium in the drinking water at concentrations ranging from 0 to 50 ppm for 105 or 280 day time periods. In the 105 day study, the effect of cadmium on urethan-induced pulmonary adenoma formation was evaluated. Urethan-induced sleeping times observed following i.p. injection of urethan after 3 weeks of cadmium exposure were not affected by cadmium indicating that chronic cadmium exposure did not alter the elimination of urethan. Pulmonary adenoma formation which was evaluated 84 days later was not affected by cadmium. The size and number of tumors remained unchanged. This suggests that the immunosuppressive actions of cadmium do not influence urethan-induced adenoma formation. In the 280-day study, the effects of cadmium on the incidence of spontaneous murine lymphocytic leukemia was evaluated. Mortality from the leukemia virus was greater in the cadmium-exposed mice. Mice exposed to 10 or 50 ppm cadmium experienced 33% more deaths from the virus. The average time till death was unaffected. It appears that the immunosuppressive effects of cadmium impair immunosurveillance mechanisms that control expression of the murine lymphocytic leukemia virus.
 ...
PMID:The effect of cadmium on chemical- and viral-induced tumor production in mice. 302 55

Female Swiss mice were exposed to lead in the drinking water at concentrations ranging from 0 to 1000 ppm for 105 or 280 day periods of time. The effect of lead on urethan-induced pulmonary adenoma formation was evaluated in the 105 day study. Urethan-induced sleeping times observed following ip injection of urethan (1.5 mg/g) after 3 weeks of lead exposure were not altered by lead indicating that lead did not affect the rate of urethan elimination. Pulmonary adenoma formation was evaluated 84 days later. Lead exposure did not affect the number of tumors produced, nor did it alter the mean tumor diameter in the lead treatment groups. This suggests that the immunosuppressive activity of lead does not enhance urethan-induced adenoma formation. In the 280 day study, the incidence of spontaneous murine lymphocytic leukemia was evaluated. Leukemia was observed in all treatment groups. Mortality was greater in the lead-exposed mice. Mice exposed to 50 or 1000 ppm lead had 41.6% and 58.3% more deaths associated with the virus. The median survival time was also reduced in the lead-exposed mice. It appears that the immunosuppressive effects of lead allow for increased expression of the murine lymphocytic leukemia virus.
 ...
PMID:The effect of lead on chemical- and viral-induced tumor production in mice. 304 Aug 44

Female Swiss mice were exposed to zinc chloride (0 to 500 ug/mL) or copper sulfate (0 to 200 ug/mL) in their drinking water for 15 weeks. After 3 weeks of the exposure period, the mice were administered urethan (1.5 mg/g) intraperitoneally. Urethan-induced pulmonary adenoma formation was evaluated 12 weeks later. Zinc exposure increased the number of adenomas produced but reduced the mean tumor diameter in the intermediate treatment groups, 50 and 200 ug/mL. Exposure to copper had no effect on tumor size or on tumor number. Weight gains in the mice were not affected by copper or zinc treatment, although a dose-dependent reduction in water consumption was observed with copper. Water consumption in mice exposed to zinc was elevated in one treatment group (50 ug/mL). Urethan-induced sleeping times, which reflect the rate of urethan excretion, were prolonged by zinc exposure but were unaffected by copper exposure. This finding suggests that zinc exposure impairs the elimination of urethan and enhances its carcinogenic activity, which is manifested by increased tumor formation.
 ...
PMID:Influence of copper and zinc on urethan-induced adenoma development in mice. 324 Jul 18


1 2 3 Next >>