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

Spontaneous and induced differentiation of murine erythroleukemia cells (strain 745A DS19 ) is reversibly inhibited by 12-O-tetradecanoylphorbol-13-acetate (TPA), a potent promoter of mouse skin carcinogenesis, and by other tumor-promoting macrocyclic plant diterpenes, but it is not by nonpromoting diterpenes. Twelve clones randomly isolated from this strain vary in their response to TPA. All clones are induced to differentiate by several compounds, the most potent of which is hexamethylene bisacetamide. In six clones TPA (100 ng/ml) caused greater than 90% inhibition of differentiation, as measured by the appearance of benzidine-reactive cells. In two clones cell differentiation was not inhibited by TPA even at concentrations as high as 1 microgram/ml. In four clones, differentiation was only partially inhibited (16 to 47%) by TPA. Clones resistant to TPA inhibition of differentiation were also resistant to structurally related tumor-promoting agents. The isolation of variant cell lines, sensitive and resistant to TPA, provides a tool for elucidating the mechanism of tumor promoter-mediated inhibition of cell differentiation.
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PMID:Heterogeneity of murine erythroleukemia cells with respect to tumor promoter-mediated inhibition of cell differentiation. 27 96

The effect of intestinal microflora on colon and breast carcinogenesis induced by 3,2'-dimethyl-4-aminobiphenyl (DMAB) was studied with the use of germfree and conventional F344 rats of both sexes. At 7 weeks of age, all animals except controls were given 20 weekly sc injections of DMAB in corn oil (100 mg/kg body wt/wk). Male animals were autopsied 15 weeks after the last injection, whereas female animals were autopsied 10 weeks after the last injection. Tumors were induced in the colons, duodena, breasts, ear ducts, salivary glands, and skin of conventional rats, and in the colons, breasts, ear ducts, salivary glands, and skin of germfree rats. No consistent difference was found in the incidence of tumors in the ear ducts, salivary glands, and skin between the germfree and conventional rats. None of the germfree rats showed duodenal tumors, whereas 13% of the female and 53% of the male conventional rats developed duodenal tumors. The incidence of intestinal tumors was lower in the germfree rats than in conventional animals. The mammary tumor incidence was lower in germfree female rats than in the conventional female rats than in the conventional females. DMAB induced fewer intestinal and breast tumors in germfree rats than in conventional rats.
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PMID:Effect of intestinal microflora on 2,2'-dimethyl-4-aminobiphenyl-induced carcinogenesis in F344 rats. 28 Jul 12

F344 rats were exposed intragastrically to two different dose levels of N-nitrosoheptamethyleneimine (NHMI) resulting in a cumulative dose of either 225 or 450 mg/kg body weight. Tumor development was followed either in situ in the NHMI-exposed animals or in tracheas and esophagi from NHMI-exposed donors after these organs were grafted to isogeneic recipients. Tumor responses in situ and in organ grafts were compared. The results showed that the process of carcinogenesis is not disrupted by the transplantation procedure. The carcinogen dose-response relationship observed in situ was also seen in the transplanted organs. At the high carcinogen dose, the tumor incidence was 100% in situ and transplanted esophagi and 20% in tracheas in situ compared to 25% in tracheal transplants. At the low dose, the tumor incidence was 36% in the esophagi in situ compared to 100% in transplanted esophagi, which suggests a greater sensitivity of the transplant system to detect the carcinogenicity of NHMI. The proportion of carcinomas to papillomas was markedly higher in transplanted esophagi. The tracheal tumor response at both NHMI dose levels showed the same trend but was too low to allow any firm conclusions.
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PMID:Tumor development in organ transplants obtained from carcinogen-exposed rats. 28 74

The neoplastic effects of administration of benzo[a]pyrene (BP) and (+/-)-trans-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene (BP 7,8-dihydrodiol) by oral intubation to noninbred female Ha:ICR mice have been determined. Under the experimental conditions, BP induced papillomas of the forestomach. BP 7,8-dihydrodiol also induced papillomas of the forestomach and was more potent than BP. In addition, administration of BP 7,8-dihydrodiol caused a large number of pulmonary adenomas and lymphomas. Butylated hydroxyanisole (BHA) added to the diet at a concentration of 5 mg/g inhibited BP-induced neoplasia of the forestomach. BHA also inhibited neoplasia of the forestomach, lungs, and lymphoid tissues that was caused by administration of BP 7,8-dihydrodiol. These data suggest that the inhibitory effect of BHA on BP carcinogenesis may entail events that occur subsequent to the formation of BP 7,8-dihydrodiol.
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PMID:Neoplastic effects of oral administration of (+/-)-trans-7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene and their inhibition by butylated hydroxyanisole. 28 84

The induction of sister chromatid exchanges (SCE) in the second postirradiation mitosis was studied in mouse 10T1/2 cells irradiated with 400 rads (4 grays) and maintained in stationary growth for several hours after x-ray exposure (similar to liquid holding recovery experiments in bacterial cells). X-irradiation with no recovery period induced few SCE. With short recovery intervals, however, the SCE frequency rose in parallel with the increase in survival, reaching a maximum increase of 2-fold after 4 hr; SCE declined with longer recovery intervals. The influence of postirradiation incubation with the tumor promoter 12-O-tetradecanoylphorbol 13-acetate (TPA) and with the protease inhibitors antipain and leupeptin was studied on spontaneous, x-ray-induced (no recovery), and recovery-induced (4 hr) SCE. TPA (0.1 microgram/ml and 1.0 microgram/ml) increased the frequency of both spontaneous and direct x-ray-induced SCE, but not of recovery-induced SCE. Incubation with the protease inhibitors suppressed both TPA- and recovery-induced SCE, but had no effect on direct x-ray-induced SCE. These results are discussed in relation to the hypothesis that promotional events in carcinogenesis may involve the expression of mutational damage in cells by mitotic segregation.
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PMID:Effect of tumor promoters, protease inhibitors, and repair processes on x-ray-induced sister chromatid exchanges in mouse cells. 28 35

Neoplastic and nonneoplastic lesions in untreated (C57BL/6N x C3H/HeN)F1 (B6C3F1) mice used as controls in carcinogenesis tests were tabulated and evaluated. The most common neoplasms in 2,543 male mice were hepatocellular adenomas and carcinomas. In 2,522 female mice, common tumors were lymphomas, leukemias, pulmonary adenomas and carcinomas, hepatocellular adenomas and carcinomas, and pituitary adenomas. The risk of developing most neoplasms increased with the age of the mouse. Hepatocellular carcinomas metastasized in 12% of the animals with these tumors. Other than lymphomas and leukemias, few other tumors metastasized. Nonneoplastic lesions included cystic hyperplasia of the uterus, nephritis, ovarian and uterine cysts, inflammatory lesions of the lung, mineralization in the brain, and focal hyperplasias in several tissues. The focal hyperplasias in lung and pituitary, adrenal, and thyroid glands were suggestive of the early stages of neoplasia. Comparative aspects of lesions in aging mice and their interpretation in carcinogenesis tests are discussed.
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PMID:Neoplastic and nonneoplastic lesions in aging (C57BL/6N x C3H/HeN)F1 (B6C3F1) mice. 28 39

12-O-Tetradecanoylphorbol-13-acetate, a potent promoter of carcinogenesis in mouse skin, enhanced differentiation of cultured mouse myeloid leukemia cells (M1) induced by human urinary protein or by lipopolysaccharide from Salmonella typhosa. 12-O-Tetradecanoylphorbol-13-acetate enhanced differentiation of all the markers tested, such as phagocytosis, Fc rosette formation, lysozyme activity, and morphological change. Other potent tumor-promoting macrocyclic plant diterpenes also enhanced the induction of differentiation, but no-tumor-promoting diterpenes did not. These findings were in marked contrast with generally accepted findings on the inhibitory effect of 12-O-tetradecanoylphorbol-13-acetate on terminal differentiation observed in other cell culture systems but consistent with the observations with some kinds of leukemia cells.
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PMID:Enhancing effect of phorbol esters on induction of differentiation of mouse myeloid leukemia cells by human urinary protein and lipopolysaccharide. 29 79

When normal mice are exposed for short periods to ultraviolet light (UV), they support the progressive growth of transplanted syngeneic UV-induced tumors. Normal nonirradiated mice almost always reject these tumor implants. The UV-mediated suppression of the antitumor response can be adoptively transferred to normal syngeneic mice with lymphoid cells derived from short-term UV-irradiated donors. Transfer of the suppressive effect is dosage dependent and also appears to require the presence of viable T lymphocytes. Suppressive activity was observed in both the spleen and thymus of UV-irradiated donors. In the preceding paper we have established that UV irradiation does not cause a general depression of testable immune functions. Collectively these data suggest that short-term UV irradiation of mice leads to an increase in suppressor cell activity, thereby causing an inhibition in the host's ability to respond to an antigenic UV-induced tumor. The possible role of this phenomenon in the mechanism of UV carcinogenesis is discussed.
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PMID:Modification of immunological potential by ultraviolet radiation. II. Generation of suppressor cells in short-term UV-irradiated mice. 30 10

Tumor development was observed for 24 months in neonatally thymectomized (nTx) and normal (C3H/HeMs x 129/J)F1 mice. Thymectomy was performed at 3 days of age. Ovarian (29%, with significant difference from the control at P less than 0.001), pituitary (6%, P less than 0.08), and lymphoreticular tumors (16%, P less than 0.05) were observed in higher incidence in nTx females compared with normal controls, resulting in a significant increase in overall tumor incidence (99 tumors in 114 nTx females vs. 37 tumors in 71 normal females, P less than 0.01). No apparent difference in overall tumor incidence was observed between nTx and non-Tx males. Also, there was no higher risk for lung, liver, and mammary tumors in males and females after neonatal thymectomy. The finding that increased tumor incidence was limited to endocrine and lymphoreticular tissues does not support the concept of immune surveillance of carcinogenesis, but rather suggests the importance of tumor-prone conditioning of endocrine or immune systems as a result of neonatal thymectomy.
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PMID:Prevalent types of tumors developing in neonatally thymectomized mice. 31 56

The relationship of aging to carcinogenesis was immunologically examined in the hamster-bovine adenovirus type 3 system. The age of animals at the time of virus inoculation influenced the tumor growth and latency period, but not the tumor incidence. The immunological competence of hamsters to sheep red blood cells became matured around 4 weeks after birth and was not affected by the infection of bovine adenovirus type 3 (BAV-3). The strength of transplant immunity was dependent on the age of animals at the time of immunization. The growth of progressive type of tumors induced by inoculation with BAV-3 into younger animals was inhibited by the repeated inoculation of excess dose of BAV-3, administration of BCG and transfer of sensitized lymphocytes during the tumor latency. The growth of non-progressive type of tumors induced by inoculation with BAV-3 into adult hamsters was accelerated by administration of antithymocyte serum or thymectomy. The tolerance to tumor specific transplantation antigens did not play a critical role in the present system. The blocking activity to sensitized lymphocytes was demonstrated in the sera taken from hamsters developing a progressive type of tumor even in the early period of carcinogenesis.
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PMID:The relationship between age-dependent immunological competence of host and tumor growth in the hamster-bovine adenovirus type 3 system. 33 64


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