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)

Biological characteristics of nodule-like alveolar lesions (NLAL) induced by 7,12-dimethylbenz[a]anthracene (DMBA) in organ culture of whole mammary gland (BALB/c female mice) were assessed after transplantation into gland-free mammary fat pads of syngeneic virgin mice. (i) Tissue-fragment explants from NLAL areas of the gland produced abnormal lobuloalveolar (LA) outgrowths in 3 of 10 fat pads. (ii) Transplantation of dissociated cells of NLAL-derived LA outgrowths into 36 fat pads showed 100% LA outgrowths and 3 (8%) of these 36 outgrowths produced mammary carcinomas. (iii) The explants of dissociated cells from whole mammary glands treated with DMBA in culture produced full or partial LA structures in 2 of 56 outgrowths. (iv) The explants of dissociated cells prepared from outgrowths derived from outgrowths derived from explants as in iii produced 9 LA outgrowths in 16 instances; mammary tumor incidence in these outgrowths was 3 of 16 (18%). (v) The explants of tissue fragments from LA outgrowths as in iv produced LA outgrowths in 20 of 20 fat pads; mammary carcinomas appeared in 16 of 20 (80%) of these outgrowths. No NLAL was detectable in control glands treated with dimethyl sulfoxide (solvent for DMBA); explants of the control glands consistently produced ductal outgrowths and no tumor. This accomplishment of chemical carcinogen-induced neoplastic transformation of epithelial cells in vitro provides a model for studying carcinogenesis in an entire isolated organ.
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PMID:Neoplastic transformation of epithelial cells in whole mammary gland in vitro. 11 56

Three-week-old female rats were fed 0.09 (zinc-deficient), 0.77 (zinc-adequate) or 3.98 (zinc-supplemented) mmol zinc/kg diet in three experimental groups and the palatal mucosa was painted with the water-soluble carcinogen 4-nitroquinoline N-oxide (4NQO) three times a week for 20 weeks. The zinc-supplemented diet seemed to retard the induction of carcinogenesis, whereas a low-zinc diet had the opposite effect. Once initial cellular changes had been induced the supplementary zinc seemed to accelerate their further advancement. Zinc-deficiency in animals fed a copper/zinc low-zinc diet was reflected in the plasma and liver zinc levels as well as in the copper/zinc ratio. The development of cancer was accompanied by a decrease in plasma zinc and an increase in the plasma copper/zinc ratio as well as in the liver zinc. These changes were most remarkable in the zinc-supplemented group.
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PMID:Influence of zinc on onset and progression of oral carcinogenesis in rats. 11 33

Histopathological studies were conducted on experimental carcinogenesis in mouse salivary glands using D L-isoproterenol hydochloride (isoproterenol) and 9 10-dimethyl-1 2-benzanthracene (DMBA). DMBA was administered once at 1 mg/0.02 ml in olive oil to the salivary glands, and isoproterenol was injected intraperitoneally at 1 mg/0.05 ml saline solution three times a week for 2 weeks at different periods during the oncogenic process. Salivary glands treated with carcinogen showed a relatively constant sequence of changes and developed epithelial and mesenchymal tumors irrespective of isoproterenol administration. Isoproterenol did not influence the development of another type of tumor; however, it did retard the oncogenic processes.
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PMID:Effects of isoproterenol on chemical carcinogenesis with DMBA in mouse salivary glands. 12 Apr 30

Living organisms have various mechanisms for repairing spontaneous and mutagen-induced damage in DNA. Mutagenesis, teratogenesis, and carcinogenesis are discussed in relation to DNA misrepair. The existence of highly efficient genetic mechanisms for tolerating environmental threats is argued from evolutionary viewpoints.
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PMID:Evolutionary considerations of DNA repair in relation to mutagenesis, teratogenesis and carcinogenesis. 12 Nov 55

The production of lung adenomas in strain A mice following multiple injections of 17 alkyl halides and of 3 base analogs was investigated. A slight but significant increase in the average number of lung tumors per mouse was noted following the administration of methyl iodide, n- and i-propyl iodide, sec- and tert-butyl chloride, i-, sec-, and tert-butyl bromide, and n- and sec-butyl iodide. The administration of comparable doses of ethyl bromide, ethyl iodide, n-butyl chloride, benzyl chloride, and 1-chloromethylnaphthalene to mice resulted in no significant increase in the frequency of lung tumors over that seen in vehicle-treated control mice. n-Butyl bromide and tert-butyl iodide similarly appeared to have no significant effect on the lung tumor frequency, but these compounds were too toxic to be tested at the high dosages used with the other alkyl halides. 5-Iodo-, 5-bromo-, and 5-fluorodeoxyuridine also appeared to have no significant effect on the lung tumor frequency. These results indicate that a high proportion of low-molecular-weight alkyl halides may be weakly carcinogenic and provide evidence supporting an electrophilic hypothesis of carcinogenesis.
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PMID:Bioassay of alkyl halides and nucleotide base analogs by pulmonary tumor response in strain A mice. 12 6

Currently N-acetoxy-N-acetyl-2-aminofluorene is favored by many investigators to be a model of the ultimate electrophilic carcinogenic agent derived metabolically from the carcinogen N-acetyl-2-aminofluprene. The model induced in vitro a delayed ATP energized increase in mitochondrial volume as indicated by the decrease in absorbancy at 520 nm. The ATP energized decrease in absorbancy was inhibited by rutamycin, 2,4-dinitrophenol and a high level of antimycin known to induce ATPase activity. The known to inhibit respiration without inducing ATPase activity. Malate or potassium ion did not affect the phenomenon, however, sulfate ion which has been implicated in liver carcinogenesis shortened the induction period. Showdomycin stimulated the phenomenon. N-Acetoxy-N-acetyl-2-aminofluorene interacts with the machinery of oxidative phosphorylation. N-Acetoxy-N-acetyl-2-aminofluorene was enzymically converted by the mitochondria to N-hydroxy-N-acetyl-2-aminofluorene. These findings extend the experimental confluence of oxidative phosphorylation with carcinogenesis.
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PMID:The disturbance of oxidative phosphorylation by N-acetoxy-N-acetyl-2-aminofluorene, a model ultimate carcinogen. 12 82

The damage and repair of rat brain DNA was studied in vivo after a single carcinogenic dose of ethylnitrosourea. Fragmentation of the brain DNA produced by this carcinogen was demonstrated on alkaline sucrose gradients. By the 24th hrs after treatment with ethylnitrosourea the single-strand damage to DNA was not completely repaired. As the highly differentiated cells of the central nervous system do not proliferate, it is possible that during brain carcinogenesis delayed repair of DNA of primitive cells might be needed for the formation of tumor anlage.
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PMID:Strand breakage in rat brain DNA and its repair induced by ethylnitrosourea in vivo. 12 17

The Growing importance of industrial noxae for carcinogenesis will, in the course of further progressive mechanization and industrialization, suggest an increasing confrontation with this problem. The above mentioned case, a patient working with insulating materials on industrial heating systems, impressevely demonstrates the transformation of chronic laryngitis into a carcinoma in the course of years, brought about by industrial influences and thus proving the exogenous origin of this genesis. Dust as well as strong effects of heat under conditions of variable atmospheric humidily are concerned to be principal damaging factors.
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PMID:[A case of industrial origin of laryngeal carcinoma (author's transl)]. 12 23

The purpose of this study was to find whether gastric resection enhances the incidence of carcinoma in the remaining part of the stomach. 66 male Wistar rats were subjected to stomach resection according to the Billroth I or the Billroth II method. These rats, as well as control animals with intact stomachs, were fed the carcinogen N-Methyl-N'-nitro-N-nitrosoguanidine (NG). -- 25 of 66 animals developed carcinomas in the gastric remnant. Precancerous lesions were seen in 18 rats. The tumours were characterized histologically as adenocarcinomas. They were almost exclusively localized in the region of the gastroenteral anastomosis. The process of tumour formation in the resected stomach was completed within 17-31 weeks on continuous administration of NG in a concentration of 120 mg/l in the drinking water. In contrast to these findings, the development of cancer in the intact stomach required on average 41 weeks under the same conditions of NG administration. However, with regard to the incidence of malignant changes, no significant difference was observed between animals undergoing the Billroth I method and those undergoing the Billroth II method.--The results suggest that the resected stomach of the rat is more susceptible to induction of cancer than the intac one. Exposure of the resected stomach to an oral carcinogen induces carcinogenesis predominantly in the anastomotic region.
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PMID:Susceptibility of the resected stomach to experimental carcinogenesis. 13 24

After subcutaneous application of 0.5 mg 3,4-benzopyrene (BP) to Sprague-Dawley-rats on the 2nd day of life, 50% of the animals developed local fibrosarcomas after 250 +/- 70 days. Additional treatment with immunostimulating (BCG, albumin, vitamin A-acid) or immunodepressive agents (hydrocortisone, cyclophosphamide, methotrexat) which was started 6 days after birth and maintained throughout life, did not influence carcinogenesis with respect to tumor incidences and induction periods of tumors.
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PMID:Experimental investigations on the influence upon the chemical carcinogenesis. IInd communication: studies with 3,4-benzopyrene. 13 32


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