Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ability of optically pure (+)- and (-)-trans-7,8-dihydroxy-7,8-dihydrobenzo(a)pyrene to initiate skin tumors in mice was determined with a two-stage tumorigenesis system. A single application of 50 to 200 nmoles of (+)- or (-)-trans-7,8-dihydroxy-7,8-dihydrobenzo(a)pyrene to the backs of CD-1 mice followed by twice-weekly applications of 12-O-tetradecanoyl-phorbol-13-acetate revealed that the (-)-enantiomer was 5- to 10-fold more potent than was the (+)-enantiomer as a tumor initiator at the three dosage levels tested. When the tumor-initiating activities of the (+)0 and (-)-enantiomers of trans-7,8-dihydroxy-7,8-dihydrobenzo(a)pyrene were compared to the activity of benzo(a)pyrene at an equimolar dose, the (-)-enantiomer was more active while the (+)-enantiomer was considerably less active. This is the first report of differences in the carcinogenic activity between optical enantiomers.
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PMID:Marked differences in the tumor-initiating activity of optically pure (+)- and (-)-trans-7,8-dihydroxy-7,8-dihydrobenzo(a)pyrene on mouse skin. 87 99

The skin-tumor-initiating abilities of various metabolites of benzo(a)pyrene (BP) were determined in mice by using a two-stage system of tumorigenesis. We previously reported that BP-7,8-dihydrodiol (+/- trans) was approximately as potent as BP, suggesting that it may be a proximate carcinogen, but the alleged ultimate carcinogen of BP [BP-7,8-dihydrodiol-9,10-epoxide (anti)] was a weak tumor initiator (Cancer Lett.2: 115, 1976). Because of its high reactivity, the tumor-initiating ability of the BP-7,8-dihydrodiol-9,10-epoxide (anti) was determined by using acetone, benzene, and tetrahydrofuran (THF) as the solvent vehicles. The 'diol-epoxide' of BP was found to be an effective tumor initiator when applied topically in THF. The effectiveness of the various vehicles for the 'diol-epoxide' was as follows: THF greater than benzene greater than acetone; however, acetone was the best solvent for BP tumor initiation. The BP-9,10-dihydrodiol and BP-3-hydroxy were found to be weak tumor initiators. BP-3-hydroxy was also tested for tumor-promoting ability and was found to be inactive in this capacity.
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PMID:Skin-tumor-initiating ability of benzo(a)pyrene-7,8-diol-9,10-epoxide (anti) when applied topically in tetrahydrofuran. 89 Jun 84

Tests were made of the effectiveness of herpesvirus of turkeys (HVT) vaccine in preventing tumorigenesis following challenge with a neoplastically transformed Marek's disease tumor cell line (MSB-1). HVT vaccine prevented tumors due to MSB-1 inoculation whereas 21.4% of unvaccinated controls had tumors. The results support, but do not prove, the theory that HVT acts through enhancement of cell-mediated immunity against MDV-transformed cells. The drawbacks of using MSB-1 cells in this experiment and the need for true Marek's transplantable tumor cells are discussed.
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PMID:Efficacy of herpesvirus of turkeys vaccine against challenge with Marek's disease tumor cells. 90 84

The ability of arene oxides, and diol epoxides of benzo(a)pyrene to initiate skin tumors in mice was determined by using a two-stage system of tumorigenesis. (+/-)-7beta,8alpha-Dihydroxy-9alpha, 10alpha-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene was a more effective tumor initiator than was (+/-)-7beta,8alpha-dihydroxy-9beta,10beta-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene when applied topically to CD-1 mice and then followed by twice-weekly applications of the promotor 12-O-tetradecanoylphorbol-13-acetate. (+/-)-7beta,8alpha-Dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene was approximately 20 to 30% as active as benzo(a)pyrene was as a tumor initiator. (+/-)-7beta,8alpha-Dihydroxy-7beta,8beta-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene, benzo(a)pyrene, 9,10-oxide, and benzo(a)pyrene 11, 12-oxide, possessed about 1, 2, and 10%, respectively, of the tumor-initiating activity of benzo(a)pyrene.
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PMID:Comparison of the tumor-initiating activities of benzo(a)pyrene arene oxides and diol-epoxides. 90 47

Hereditary adenomatosis of the colon and rectum (ACR) and its Gardner's syndrome variant, an autosomal dominant trait, indicate a propensity for neoplasia. The present study describes the growth abnormalities of cultured human skin fibroblasts derived from normal-appearing cutaneous biopsies of ACR genotypes and a portion of the clinically asymptomatic ACR progeny, first filial generation, and their differential susceptibility to transformation by Kirsten murine sarcoma virus. These skin fibroblasts, but not cells derived from unaffected individuals, showed lack of contact inhibition, decreased serum requirement for growth, elevated levels of plasminogen activator, and alterations in the intracellular distribution of actin cables; they did not, however, grow in the absence of anchorage, nor did they form palpable tumors in congenitally athymic BALB/c nu/nu mice, and they were normal with regard to cholesterol feedback regulation. Skin fibroblasts from ACR subjects were 100- to 1000-fold more susceptible to transformation by the Kirsten murine sarcoma virus than were normal cells. The virally transformed skin fibroblasts were anchorage-independent and formed tumors in athymic mice. These growth abnormalities represent steps in the changing phenotypic expression of cells undergoing neoplastic transformation. Identification of abnormal expressions associated with oncogenesis may facilitate their use as diagnostic indices for the detection of latent forms of colon cancer in man.
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PMID:Phenotypic markers in human skin fibroblasts as possible diagnostic indices of hereditary adenomatosis of the colon and rectum. 92 93

The gross, light and electron microscopic features of a pineocytoma of the Syrian hamster (mesocricetus auratus) which had been induced by a human oncogenic virus (JC papovavirus) have been defined. For comparison, adult hamster pineal tissue was studied, and the literature was consulted in regard to other pineal parenchymal tumors, and to pineal cell differentiation during ontogeny and phylogeny. Many differentiated tumor cells contained organelles, such as vesicle-crowned lamellae (synaptic ribbons) and microtubular sheaves, as consistent with adult hamster pineocytes. Some cells showed rudimentary photoreceptor-like differentiation as consistent with fetal hamster pineocytes and with cells seen in the pineal systems of some lower vertebrate species. Such tumor cells had lumen-directed specialized cytoplasmic extensions which, by their richness in mitochondria and presence of centrioles and striated rootlets, resembled inner segments. Extending 9+0 cilia were accompanied by occasional lamellar whorls. Oncogenesis seems to have simulated different stages of hamster pineal ontogeny. This observation would support the theory that the secretory mammalian pineocyte derived phylogenetically from the true photoreceptor cell of the pineal system of fishes and amphibians. The possible influences of host and of virus in the accomplishment of tumor morphology were discussed. This tumor differed considerably in pattern and cell detail from the only other pineocytoma studied previously by electron microscopy. It is the first experimentally induced pineocytoma.
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PMID:Experimental pineocytoma of the Syrian hamster induced by a human papovavirus (JC). A light and electron microscopic study. 94 81

An experimental approach to the immunoprophylatic control of feline oncornavirus-mediated diseases has included induction of antivirus immunity and antibodies to the feline oncornavirus-associated membrane (tumor) antigens. A suitable model for exploring the effectiveness of killed oncornavirus vaccines in the cat has been provided by the use of feline sarcoma virus. Immunization of seven pregnant queens over a 6-week period with ultraviolet light-inactivated Gardner-Arnstein feline sarcoma virus resulted in significant protection among 12 kittens challenged with a tumor-forming Dose 90 at 7 days of age. This immunity was not present in kittens challenged at 35 days of age. Among 12 kittens born of queens immunized during pregnancy with ultraviolet light-inactivated Kawakami-Theilen feline leukemia virus and challenged with the same live virus at 4 days of age, significant protection was noted, ranging from prolongation of survival time to complete protection in 3 kittens. In general, the higher the antibody titer in the mother, the more effective the protection afforded the kittens. Immunization of 43 kittens during their first 5 weeks of life with the same vaccines used in adult cats did not immunize sufficiently to protect against feline sarcoma virus challenge at 5 weeks of age. Neutralizing antibody responses in these kittens were significantly lower than in pregnant queens. That kittens of this age are immunologically responsive was established, since complete protection of 9 kittens to feline sarcoma virus was obtained by immunization with a crude tumor extract inactivated with 5 to 7 megarads of gamma-irradiation. All these kittens developed feline oncornavirus-associated membrane antibodies while 3 developed demonstrable levels of virus-neutralizing antibodies. The results of these studies are believed indicative that killed virus vaccines and tumor vaccines can be effective immunoprophylatic measures in the control of RNA tumor virus oncogenesis in the cat. Developments in this model system should be relevant to any consideration given similar vaccines in humans.
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PMID:Experimental oncornavirus vaccines in the cat. 94 34

DNA synthesis in mammary gland estimated by [3H]thymidine incorporation was significantly higher on the day of proestrus than on the second day of diestrus in 50-day-old female Sprague-Dawley rats. The percentage of progressive mammary tumors, tumor growth rate, and the number and the weight of tumors per tumor-bearing rat were significantly higher in the animals given a single i.v. injection of 5 mg 7,12-dimethylbenz(a)anthracene at proestrus than in the animals given it at diestrus. Inhibition of DNA synthesis at proestrus by 2-bromo-alpha-ergocryptine also suppressed mammary tumorigenesis by the carcinogen. In 90-day-old rats in which little difference was found in mammary gland DNA synthesis between proestrus and diestrus, there was no difference in mammary tumorigenesis between animals given the carcinogen at proestrus and animals given it at diestrus. On the other hand, the prestimulation of mammary gland DNA synthesis by prolactin increased the growth, the number, and the weight of carcinogen-induced mammary tumors. These results demonstrate the importance of mammary DNA synthesis at the time when a carcinogen acts on the glands in mammary tumorigenesis.
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PMID:Importance of mammary gland DNA synthesis on carcinogen-induced mammary tumorigenesis in rats. 94 23

Histologically confirmed testicular tumors were diagnosed in 410 dogs from 12 North American veterinary university hospitals and clinics. Three tumor-cell types, Sertoli cell tumor, interstitial cell tumor and seminoma, were about equally represented. Several breeds were identified with high risk for different testicular tumor-cell types. Cytogenetic and immunogenetic studies of these dog families could offer leads applicable to familial testicular cancer in man. The multiplicity of breeds within the series suggests that, as in man, other factors, in addition to hereditary, play a role in etiology. Cryptorchid dogs appear to have a 13.6 times higher risk of testicular tumor than normal dogs. Additionally, male dogs with an inguinal hernia have an increased risk (4.7) of testis tumors. There were no detectable excesses of other urogenital anomalies or urogenital tumors among the series. The Shetland Sheepdog is suggested as an appropriate model for research into the mechanisms responsible for testicular maldescent and tumorigenesis.
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PMID:Canine testicular tumors: epidemiologic features of 410 dogs. 97 90

Natural anti-tumor antibodies (NAA) were revealed, by a complement-dependent cytotoxicity test on el4 lymphoma cells, in the serum of C3Hf but not of C57BL mice. Hybrids between the positive C3Hf and the negative C57Bl mice were NAA producers. Individual variability of NAA level was found in C3Hf and in the hybrids. The study of mice housed in the same or in different cages and of mice belonging to the same or to different litters demonstrated a randomly distributed variability. These observations seem to exclude environmental influences on the natural immune response or genetic mutations in the C3Hf strain with the appearance of variants with different NAA content. The NAA level was age-dependent with a peak around 20-24 weeks of age. Inoculum of lymphoma cells induced an increase in the NAA level both in C3Hf and in the hybrids but not in C57Bl mice which seem therefore incapable of making guinea-pig complement-fixing NAA. The individual variability of NAA level and the stimulating effect of tumor cells support a potential role of NAA in immunosurveillance of oncogenesis.
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PMID:Natural antibodies directed against murine lymphosarcoma cells: variability of level in individual mice. 98 42


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