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)

Intermittent implantation of 600--1,300 microgram estriol subcutaneously beginning 48 h before oral administration of 7,12-dimethylbenz(a)anthracene or procarbazine prevents development of 80--90% of carcinomas of the breast occurring during the natural life span of the intact female Sprague-Dawley rat. Some estriol precursors were less inhibitory of breast cancer development among 23 other estrogens and androgens, progestins and glucocorticoids tested. More frequent or lower estriol doses than 100--200 microgram/kg/24 h every 2 months were less inhibitory of breast carcinogenesis. No other types of neoplasms were reduced in incidence by estriol implants, which also reduced uterine weights by 20--25%. Intermittent substitution of estriol for estrone or estradiol in the nuclear receptor complexes of target cells probably accounts for these observations, which resemble the effect of castration in reducing breast cancer incidence. Human studies indicate excellent tolerance for oral estriol doses of 10--200 microgram/kg/24 h, which may correct subnormal estriol/estrone + estradiol urinary quotients associated with elevated risk of breast carcinogenesis in epidemiologic investigations.
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PMID:Clinical and experimental aspects of the anti-mammary carinogenic activity of estriol. 9

Changes of the cell cycle during carcinogenesis of hamster cheek pouch epithelium were studied and it was demonstrated that in hyperplastic and neoplastic stages, the cell cycle time decreased to approximately 2/3 and 1/3 of the normal control, respectively. A nominal growth fraction was found to exceed unity in carcinogen-treated epithelium, whether hyperplastic or neoplastic. This result seems to indicate that a considerable number of cells in which DNA synthesis is stimulated by the carcinogen fail to enter mitosis. A possible implication of repair synthesis is also discussed.
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PMID:Changes of the cell cycle during carcinogenesis of hamster cheek pouch epithelium by 7,12-dimethylbenz[a]anthracene. 9 14

Light and electron microscopy studies of lactic dehydrogenase activity were carried out in embryonic, neonatal, and adult mouse lungs and in lungs undergoing chemically induced carcinogenesis. Embryonic mouse lungs were collected on the 6th, 12th, and 18th days of gestation; 1-day-old lungs were used for the neonatal model. These were compared with adult normal mouse lung and lungs of the animals treated with 4-nitroquinoline 1-oxide at a monthly interval until cancer developed. Enzymatic activity was seen in the embryonic, precancerous, and malignant lung tissues and was found diffusely in the cytoplasm of the epithelial cells.
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PMID:Histochemical and ultrastructural study of lactic dehydrogenase in chemically induced lung cancer. 9 29

The distribution of 4-nitroquinoline 1-oxide (4-NQO) reductase, assumed to be closely related to the carcinogenesis of 4-NQO, was investigated in the mucosa of canine digestive tract, and its results indicated following points. 1) The activity of 4-NQO reductase was highest in the esophagus, next in the stomach, and remarkably low in the small and large intestines. 2) There is no significant difference in the 4-NQO reductase activity between the upper, middle, and lower portion of the esophagus, but its activity was higher in the female than in the male in its upper and middle portions. 3) Among the esophageal tissue, its activity was high only in the mucous epithelium and very low in all other layers. 4) Most of the enzymic activity in the esophageal mucosa existed in the cytosol fraction and activity of the microsome fraction was remarkably low. Even if NADPH or NADH was used as the hydrogen donor, its activity was not different in the cytosol fraction, but the former was a better hydrogen donor in the microsome fraction. 5) In the gastric mucosa, the enzymic activity was equally high in various portions of the corpus ventriculi; the greater and lesser curvatures, anterior and posterior parietes, and fundus. It was remarkably low only in the pyloric antrum.
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PMID:Distribution of 4-nitroquinoline 1-oxide reductase in the mucosa of canine digestive tract. 9 82

DNCB is an antigen that stimulates the cell-mediated response in a sensitized host. The purpose of this study was to define the effect DNCB would have on a standard model system for oral carcinogenesis, theorizing that tumorgenesis would be delayed or inhibited. Fifty-six Syrian hamsters were divided into four groups. In group A (DNCB/DMBA), the right buccal pouch of twenty animals was treated with 2% DNCB in orabase, twice a week, and 0.5% DMBA, three times a week, for 10 weeks. In group B, twenty animals received DMBA only. In group C, six animals received DMBA in Orabase. In group D, ten animals received DNCB in Orabase only. The animals were killed at 6, 12, 16, and 20 weeks. The results indicate that there were no differences in the latent period or in the histologic characteristics of the epidermoid carcinomas that developed. However, there was sensitization of the buccal pouch in pouches painted with DNCB, in that gross and histologic evidence of a delayed sensitivity reaction was demonstrated.
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PMID:The effect of dinitrochlorobenzene (DNCB) on dimethylbenzathracene (DMBA) carcinogenesis on hamster buccal pouch. 10 32

The present study was done to ascertain whether a specific carcinogenic agent has a causal effect on the initial proliferation of only one cell type or whether it acts indiscriminately on all cells in the breast secretory unit. Enzymes histochemistry and electron microscopy were performed on DMBA-induced mammary tumors in female Sprague-Dawley rats and on virus-associated spontaneous mammary tumors in C3H/HEJ mice. The results showed that the chemical carcinogen DMBA affects initial myoepithelial cell proliferation, while virus-associated mammary carcinoma originated from ductular epithelial cell proliferation. To determine whether a specific tumor is composed of a single cell type, tumors were grown in tissue culture. The monolayer was fixed in the usual manner for electron microscopy while in Falcon tissue culture plates. The plates were dissolved in xylene and the monolayer was cut into small pieces and embedded in the plastic media. Electron microscopy performed on the tissue culture and the original tissue from the virus-induced tumors showed the presence of viruses in large numbers. It also suggested the differentiation of basal membrane to form basal lamina and apical plasma membrane into microvilli. This study strongly suggests the presence of selective cell carcinogenesis in the mammary gland.
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PMID:A proposed selective cell carcinogenesis in mammary tumors. 10 7

The classical 2-stage carcinogenesis experiment has been modified in that the carcinogen DMBA was applied to pregnant mother animals at different dose levels and different time intervals during pregnancy. Promotion with the phorbol ester TPA was performed as usual by application of the promoter on the back skin of mice of the F-1 generation. It can be shown that it is possible to initiate fetal epidermal cells by transmaternal route and to promote them to produce visible skin tumors post natum. Tumor promotion by TPA is not restricted to the epidermis, since a broad spectrum of tumors of internal organs can be demonstrated in the initiated and promoted animals. This more general promoting activity of TPA--which implies its absorption and distribution throughout the whole body--has not yet been described. In addition, especially sensitive phases during fetal life with regard to initiation of cells by the carcinogen can be demonstrated. These phases comprise the last third of pregnancy and coincide with a high proliferative activity and the onset of differentiation of the fetal epidermis. The results emphasize the important role of prenatal carcinogenesis and demonstrate the increased risk also to the human organism by either prenatal initiation or postnatal promotion.
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PMID:Transmaternal modification of the Berenblum/Mottram experiment in mice. 10 83

The effect of deoxycholic acid on 7,12-dimethylbenz(a)anthracenecroton oil carcinogenesis in mouse skin was tested. Painting deoxycholic acid in addition to croton oil during promotion resulted in the earlier appearance of tumors, a greater tumor incidence, and a larger number of tumors per animal. DMBA initiation followed by either deoxycholic acid or solvents during the promotion period produced no tumors. Animals receiving deoxycholic acid or solvents alone developed no tumors.
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PMID:Effect of deoxycholic acid on 7,12-dimethylbenz(a)anthracene-induced, two-stage mouse skin carcinogenesis. 10 72

The effect of levamisole on DMBA-induced carcinogenesis in the cheek pouch of the hamster was studied. Findings indicate that levamisole modified the response of the pouch to DMBA at six weeks, while this effect was not maintained after 12 weeks of DMBA application.
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PMID:The effect of levamisole on DMBA-induced carcinogenesis in the hamster cheek pouch. 10 23

Male inbred Leeds strain rats were given single intragastric doses of 1200 mg/kg of 3'-methyl-4-dimethylaminoazobenzene, autoprotective against liver necrosis and then sacrificed at intervals up to 14 months. About 40 per cent of the animals died, apparently as a result of pancreatic necrosis, between 9 and 13 days after treatment while the remainder survived until they were killed. The liver changes induced included an early intense ductular cell reaction, presistent hepatocellular abnormalities and at later stages, cholangiofibrosis and increasing numbers of parenchymal clear cells. Although no tumours arose as a result of treatment, the observed histopathological changes are similar to those seen during liver carcinogenesis induced by a variety of carcinogens and may be due specifically to the carcinogenic action of the azo dye.
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PMID:Histopathology of the rat liver following a single autoprotective dose of 3'-methyl-4-dimethylaminoazobenzene. 10 11


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