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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prophylactic effect of repeated intravenous administrations of oil-attached BCG cell-wall skeleton (BCG-CWS) on the induction of tumor by 7,12-dimethylbenz[a]anthracene (DMBA) was investigated in various strains of mice. The subcutaneous injection of DMBA emulsified in oil induced squamous cell carcinoma in almost all of the strains of mice. Treatment of C57BL/6, BALB/c, and ddO strains with BCG-CWS with appropriate route and timing resulted in the retardation of DMBA-induced tumor development manifested by a prolonged latent period of tumor outgrowth. In contrast, the same BCG-CWS treatment of C3H/He and BTK mice was incapable in preventing such DMBA-induced carcinogenesis. Thus, the treatment with BCG-CWS was effective for preventing the DMBA-induced carcinogenesis in certain strains of mice, but the effectiveness varied depending on the strain. The implication of such a strain variationof the BCG-CWS effect on the prophylaxis of chemical carcinogenesis was discussed in the context of differences in the magnitude of immunopotentiation of the host by BCG-CWS.
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PMID:Prophylactic effect of BCG cell-wall skeleton on the tumor induction by 7,12-dimethylbenz[a]anthracene in mice: strain difference. 10 42

The effects of a vitamin A analog, TMMP ethyl retinoate [or ethyl-9-(4-methoxy-2,3,6-trimethylphenyl)-3,7-dimethyl-trans-2,4,6,8-nonatetraenoate] (abbreviated Ro 10-9359), and an anti-inflammatory steroid, fluocinolone acetonide (or 6 alpha, 9 alpha-difluoro-11 beta, 16 alpha, 17,21-tetrahydroxypregna-1,4-diene-3,20-dione cyclic 16,17-acetal) (abbreviated FA), given alone or together were studied in a two-stage carcinogensis system. The phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) was used as the tumor promoter in a 7,12-dimethylbenz[a]anthracene (DMBA)-initiated mouse skin system. Two stocks of female mice, CD-1 and Sencar, which differ in their degrees of sensitivity to skin carcinogenesis, were used. A dose-dependent inhibition of carcinogenic expression, as determined by a decreased number of papillomas per animal, was observed in each mouse stock with the use of both FA and Ro 10-9359 when given alone. When FA and Ro 10-9359 were given together, an enhanced effect on the lowering of tumor incidence was noted. FA effectively inhibited tumor formation in the sensitive mouse stock even when the steroid was given 1 day prior to TPA treatment under conditions of unusually high doses of initiator (DMBA) and/or promoter (TPA). These results suggest that both anti-inflammatory steroids and retinoids inhibit tumor promotion and can be effectively used as a combination regimen for increased chemopreventive response.
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PMID:Inhibition of phorbol ester-induced tumor promotion in mice by vitamin A analog and anti-inflammatory steroid. 11 Sep 70

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

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

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

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

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

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

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

The 3,4-Benzopyrene (3,4-BP) carcinogenesis can be postponed or even completely inhibited in the presence of Putrescine (P). A single s.c. injection of 2.52 mg 3,4-BP in 0.5 ml tricaprylin on female mice (NMRI-strains, 4--5 weeks old, 20--25 g of body weight) induced locally malignant tumors (sarcomas and carcinomas) up to 97% of the animals treated. (132 mice with tumors from 136 animals treated). Animals injected with 3,4-BP plus 10 mg putrescine showed a considerable reduction of tumor incidence. Only three from 38 mice treated developed tumors (8%). The prevention of tumor could not be further improved with higher putrescine amounts, for example 15 mg and 20 mg P. These concentrations were moreover toxic to the animals. Histologically, the tumors developed in the presence of putrescine were rather poor in malignant cells and mitoses were also rare, in contrast to the usual 3,4-BP tumors which were rich in polymorph cells and mitoses.
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PMID:Prevention of 3,4-benzopyrene carcinogenesis in presence of putrescine. 13 15


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