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

Aluminium chloride was subcutaneously administered to mice and its effect on the activities of 4-nitroquinoline 1-oxide (4-NQO) reductase and 4-hydroxyaminoquinoline 1-oxide (4-HAQO) reductase, and the organ distribution of carcinogen(s) in mouse lung and liver were examined. Subcutaneous administration of aluminium chloride in mice results in significant elevation of 4-NQO reductase and 4-HAQO reductase activities in their lung and liver, compared with those of the control. Simultaneous subcutaneous administration of aluminium chloride with 4-nitroquinoline[5, 6, 7, 8, 9, 10-14C] 1-oxide (14C-4-NQO) and examination of radioactivity distribution in the lung and liver showed that the radioactivity per tissue, 0.5 and 1 hr after the administration, decreased in the lung but inversely increased in the liver. Radioactivity in the lung and liver 2 hr after the administration was not different from that of the control. Simultaneous subcutaneous administration of 14C-4-NQO and aluminium chloride resulted in decreased distribution of 4-NQO and 4-HAQO in the lung compared with that of the control, while the distribution of their metabolites, 4-aminoquinoline 1-oxide (4-AQO) and 4-hydroxyquinoline 1-oxide (4-OHQO), inversely increased. Distribution of 4-aminoquinoline (4-AQ) and 4-hydroxyquinoline (4-OHQ) in the lung was not different from that of the control. These results suggest that the rapid metabolic changes of carcinogenic 4-NQO and 4-HAQO to noncarcinogenic substance(s) and decrease in the concentration of carcinogenic substances in the lung by the subcutaneous administration of aluminium chloride constitutes one of the factors for the mechanism of the suppression of carcinogenesis by aluminium chloride.
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PMID:Effect of aluminium chloride on metabolism of 4-nitroquinoline 1-oxide. 11 94

The life history and histopathology of UV light-induced skin tumors were studied in NMR rats, outbred female Swiss mice, and Syrian golden hamsters. High intensity UV light of medium wavelengths produced hyperplasia and papillomas, as well as a dysplastic, intermediary solar keratosis-like stage, with distinct cellular atypia leading to several types of squamous cell carcinomas. High doses of UV irradiation of short duration caused scars, which developed into fibromas and fibrosarcomas composed of "light" and "dark" cells. Carcinomas with neoplastic squamous and fibrous components were uncommon; however, collision tumors with two components were occasionally seen. Angiomas and angiosarcomas with a proliferating endothelial structure were observed, but adnexal tumors, with follicular or sebaceous differentiation, and basal cell carcinomas were infrequent. Pigment cell tumors were found only rarely. The number of tumors and tumor-bearing animals at different stages of the experiment were also studied. Tumors were compared with lesions induced by chemical carcinogens in different systems. UV carcinogenesis was characterized by many tumor-bearing animals, but with a low total tumor count and a high mortality, thereby decreasing the number of animals-at-risk. The tumor types, their progression from on type to another, and the distribution of certain biologic characteristics were also analyzed. We concluded that UV irradiation is an effective tumor inducer in animal skin, and the type of tumor, its behavior, and location depend on the experimental conditions.
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PMID:Life history and histopathology of ultraviolet light-induced skin tumors. 11 77

The effects and site(s) of action of progesterone on DMBA mammary carcinogenesis in the rat, when a small dose of the carcinogen was applied directly to the inguinal mammary gland, were investigated. No reduction in tumour yield was apparent when progesterone was administered s.c. for 18 days before dusting DMBA. This finding contrasts with a previously reported inhibitory effect on carcinogenesis when hormone treatment was followed by intragastric administration of DMBA. When progesterone injections were begun either 2 days before or 2 days after direct application of DMBA, and were continued until the end of the experiment (135 or 195 days) an enhancement in carcinogenesis was observed similar to that previously demonstrated after gastric intubation of DMBA. These findings, together with previously reported observations, suggest that progesterone may exert its inhibitory effect on carcinogenesis by acting at a site outside the breast, perhaps on the liver. However, it is likely that the hormone acts directly on the mammary tissue to exert its enhancing effect on tumorigenesis.
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PMID:Effects of progesterone on mammary carcinogenesis by DMBA applied directly to rat mammae. 11 24

An antibody to benzo[alpha]pyrene (BP) was prepared. The isolated antibody showed a specificity for BP and a low reactivity with another carcinogenic hydrocarbon, 7,12-dimethylbenz[alpha]anthracene (DMBA). The BP-antibody inhibited the in vitro cytotoxic and mutagenic activity of BP in both a rat embryo fibroblast- and a rat lung cell-mediated mutagenesis system. A possible correlation of these in vitro findings to the in vivo carcinogenesis situation is discussed.
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PMID:Benzo[alpha]pyrene antibody inhibition of benzo[alpha]pyrene-induced mutageneis. 11 82

It has been reported that twice-weekly i.p. injections of 4 mg phorbol for 10 weeks, after a single feeding of 6 mg dimethylbenz(a)anthracene (DMBA) in female Wistar rats, led to a significant augmentation of mammary adenocarcinoma incidence and of lymphatic leukemia incidence as compared to 6 mg DMBA alone. In an experiment reported here, in female Sprague-Dawley rats, using the same doses of DMBA and phorbol and the same injection schedule, phorbol given after DMBA did not augment mammary adenocarcinoma incidence or lymphatic leukemia incidence as compared to DMBA given alone. It thus appears that there is a strain-related sensitivity between Wistar and Sprague-Dawley rats with regard to the promoting activity of phorbol when phorbol treatment follows DMBA treatment, and mammary adenocarcinoma incidence and lymphatic leukemia incidence are studied. Further, in Sprague-Dawley rats, phorbol did not promote mammary fibroadenoma incidence in DMBA-treated rats, mammary adenocarcinoma incidence in procarbazine-treated rats, and mammary adenocarcinoma incidence or mammary fibroadenoma incidence in X-ray-treated rats. DMBA and procarbazine, with or without phorbol, tended to induce more mammary neoplasms in the anterior (thoracic) than in the posterior (abdominal) mammary glands. X-irradiation tended to induce mammary neoplasms in approximately equal numbers in the anterior and posterior mammary glands. It was suggested that regional differences in chemically induced mammary carcinogenesis were due to a difference in the transport and delivery of the chemical carcinogens to the regions rather than a difference in the amount of mammary gland tissue in the regions. An analysis of the numbers of Sprague-Dawley rats that developed either no mammary neoplasms, or only mammary adenocarcinomas, or only mammary fibroadenomas, or both mammary adenocarcinomas and mammary fibroadenomas in response to DMBA, procarbazine, and X-ray, suggested that the development of a mammary adenocarcinoma or the development of a mammary fibroadenoma are independent processes.
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PMID:Apparent rat strain-related sensitivity to phorbol promotion of mammary carcinogenesis. 11 89

In tissues of non-lineal rats receiving dimethyl amino-azobenzene (DAAB) or its non-carcinogenic analog diethyl amino-azobenzene (DEAB) there was found, using rabbit serum against an artificial complex RNA + MBSA (methylated bovine serum albumin), the RNA-haptene in the reaction of counter-immunoelectrophoresis in the liver and serum of rats in definite terms since the start of DAAB administration. RSR reaction and immunoelectrophoresis have demonstrated the presence of circulating antibodies against hepatic cell RNA. The kinetic of antibodies against RNA is characterized by their increase after 15 DAAB injections, their decrease to the 60th day and again an increase by the time of the tumor appearance. It is suggested that the phenomena of sensibilization and desensitization to the antigens arising in the process of carcinogenesis play a definite role in "cancelling" the antitumor immunity.
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PMID:[Immunological study of rat liver RNA in the early stages of hepatic carcinogenesis]. 11 37

Daily administration of a brominated triphenylethylene (TBP), to rats which received 20 mg of DMBA p. o. inhibits mammary carcinogenesis. The effect appears even with very small doses (i ppm in the diet) and seems to be dose related. With one exception (an adenofibroma) the tumours in control and treated animals were malignant. Administration of TBP prevents the appearance of corporea lutea in the ovaries but not the usual necrosis of the adrenal cortex.
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PMID:Inhibition of mammary carcinogenesis of dimethylbenzanthracene treated rats with a brominated triphenylethylene. 11 93

Experiments in rodents indicate that during the post-embryonic period of prenatal development, the fetus is more sensitive than the adult to certain carcinogens, by several decimal orders of magnitude. Most such agents are direct-acting and independent of metabolism. To other substances, often those which require enzyme-mediated metabolic conversion to a chemically reactive derivative in order to effect carcinogenesis, the fetus may be less vulnerable than the adult. The neonate is also more susceptible than adults to some carcinogens, and may be more susceptible than the fetus to certain agents. Both rodent and primate studies indicate that gravid females are also at elevated risk for carcinogenesis, in part because of the presence in the placenta of trophoblastic tissue which may become malignant. The contributions of rapid growth rate, changing metabolic competence, and tissue differentiation to elevated perinatal susceptibility to carcinogens in rodents and primates are discussed, together with the implications of these findings for human beings subjected to industrial or environmental exposures to such chemicals.
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PMID:Perinatal period and pregnancy: intervals of high risk for chemical carcinogens. 11 42

Of 27 lesions induced in Syrian golden hamsters by 12 applications of 0.5% 7,12-dimethylbenz[a]anthracene in liquid paraffin, 14 showed a static phase of at least 28 days' duration in their life history. Ten static lesions resumed growth, and this was accompanied by clinically obvious vascularization in 8 cases, 7 of which culminated in carcinomas by the end of the study. Because the wall of the normal hamster cheek pouch possesses small nodules whose histologic structure closely resembles that of hyperplastic epithelium, they could be misinterpreted as a product of carcinogenesis.
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PMID:Vascularization of premalignant lesions in carcinogen-treated hamster cheek pouch. 11 96

Parenchymal hepatocytes isolated from adult rats were cultured on three types of collagen-containing substrata: collagen-coated plates, collagen membranes and confluent diploid human fibroblasts. Hepatocytes on the latter two substrata maintained characteristic morphology for at least 10 days in culture, whereas degenerative changes (cell death and formation of multinucleated hepatocytes) and growth of nonparenchymal elements were seen after 5 days in cultures on collagen-coated plates. Parallel findings were seen on basal and induced levels of cytochrome P-450 and NADPH-cytochrome C reductase. The basal levels of cytochrome P-450 were not measurable after day 3 in hepatocytes cultured on collagen-coated plates, whereas measurable levels were maintained in the hepatocytes cultured on the other two substrata. Addition of phenobarbital or methylcholanthrene at day 5 in culture caused an increase in cytochromes P-450 and P-448, respectively, only in hepatocytes cultured on collagen membranes and confluent fibroblasts. Analogous results were seen for the enzyme NADPH-cytochrome C reductase. The similarities in performance between hepatocytes on collagen membranes and on human fibroblasts show that a continuous collagen-containing substratum is important for optimal performance of hepatocytes in primary culture. The possible importance of cultures of hepatocytes on human fibroblasts for carcinogenesis studies is discussed.
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PMID:Primary cultures of hepatocytes on human fibroblasts. 11 6


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