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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of oncogene was proved in 1969 with avian sarcoma virus B77. Since then, the first oncogene was identified as src gene and many other oncogenes have been found and characterized in various sarcoma and acute leukosis viruses. These oncogenes have cellular counterparts called "c-onc"s. They appeared to be the origins of viral oncogenes and some of them were actually proved to be oncogenic after coupling with viral LTR or insertion into retroviral genome. The importance of activation of c-onc in general carcinogenesis was discussed in relation to recent advances in human cancer gene study.
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PMID:[Development of oncogene study]. 630 88

Cells cultured from explants of adult rat adrenal cortex are spindle shaped and divide rapidly in media with 10-25% fetal bovine serum (FBS), but are epithelial-like and stationary in 3-6% horse serum (HS). Fully transformed Kirsten murine sarcoma virus (KiMSV)-infected cells lose this differential response to serum. To determine at what stage in the transformation process this loss occurs, cultures in passages 1-2 were infected with KiMSV, propagated for up to 30 weeks in FBS, and parallel cultures were transferred to HS prior to transformation, within 4 weeks after appearance of foci, or after complete transformation (exhibiting altered culture morphology, increased growth rate and tumorigenicity). In 7 lines grown in FBS, foci appeared 1-14 weeks post-infection and most cultures were completely transformed 1-3 weeks thereafter. Substitution of HS for FBS prior to focus formation caused partial reversion to epithelial-like morphology and reduction in growth rate. Transformation was delayed or prevented altogether, but could be elicited by addition of 1% FBS to HS. HS-substitution within 4 weeks after appearance of foci caused regression of foci, slowing of growth, and delays of complete transformation lasting up to 5 months. In three lines, HS effects on cell shape and on proliferation were dissociated, suggesting separate controls of these two parameters. HS-substitution after complete transformation did not reduce growth or reverse morphologic changes. The results indicate that, in some cases, transformation by acute oncogenic retroviruses is a multistep process involving epigenetic regulation, and that autonomy from environmental controls is acquired gradually by the infected cells. The results also demonstrate that acute transforming retroviruses can cause prolonged latent infections, the phenotypic expression of which depends on environmental factors.
Carcinogenesis 1984 Feb
PMID:Development of serum independence in Kirsten murine sarcoma virus-infected rat adrenal cells. 632 Oct 49

Seventeen nickel compounds were administered to Fischer-344 rats (N = 270) by intrarenal injection (7 mg Ni/rat); the compounds included nickel sulfides, selenides, arsenides, oxide, antimonide, telluride, titanate, ferronickel alloy and metallic nickel dust. Erythrocytosis, as defined by peak hematocrit values that averaged greater than 55% during 1-4 months post-injection, occurred in nine of 17 Ni-treated groups (NiS2, beta NiS, alpha Ni3S2, Ni4FeS4, NiSe, Ni3Se2, NiAsS, NiO, Ni dust). Renal cancers (N = 23) developed within 2 years post-injection in nine of 17 Ni-treated groups (NiS2, beta NiS, alpha Ni3S2, Ni4FeS4, NiSe, Ni3Se2, NiAsS, NiAs, NiFe alloy). The renal cancers included eight fibrosarcomas, five mesangial cell sarcomas, two renal cell carcinomas, two carcinosarcomas, two leiomyosarcomas, two undifferentiated sarcomas, one rhabdomyosarcoma and one nephroblastoma. No erythrocytosis or renal cancers occurred in control rats (N = 97) in three groups treated with the vehicles or metallic iron dust. Rank correlation (p less than 0.0001) was observed between the incidences of erythrocytosis and renal cancers in the 17 Ni-treated groups. Rank correlation (p less than 0.001) was observed between the present incidences of renal cancers and the sarcoma incidences previously reported following intramuscular administration of the 17 nickel compounds to Fischer-344 rats (14 mg Ni/rat). The incidences of renal cancer were not correlated with the mass-fractions of nickel in the 17 compounds, the dissolution half-times of the compounds in rat serum or renal cytosol, or the phagocytic indices of the compounds in rat peritoneal macrophages.
Carcinogenesis 1984 Nov
PMID:Association between erythrocytosis and renal cancers in rats following intrarenal injection of nickel compounds. 648 75

The results of combined treatment of CBA female mice with 1,2-dimethylhydrazine (DMH) and estradiol dipropionate (EP) are discussed in terms of a two-stage carcinogenesis hypothesis. 20% of mice treated with DMH alone developed uterine sarcomas. EP given after the cessation of DMH-treatment increased sarcoma incidence as high as 60.6% (5 micrograms EP) or 66.7% (10 micrograms EP) and significantly decreased the time of the first tumour appearance. From the standpoint of the two-stage carcinogenesis it is considered possible for EP to influence the tumour-initiating stage.
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PMID:[Analysis of uterine sarcoma induced in mice in terms of the two-staged development of tumors]. 651 Mar 29

Struma maligna raises some questions concerning carcinogenesis, precancerosis, as well as diagnosis, therapy and prognosis. Only little information can be obtained by evaluating morphological criteria. Usually exhibiting modest malignancy papillary carcinoma as well as C-cell-carcinoma of the thyroid deserve particular interest. With regard to the velocity of growth (organoid arrangement of tumour tissue), also folliculoid carcinoma (i.e. Struma Langhans) will differ from so-called 'true' carcinomas characterized by a slower rate of growth. All other types of carcinoma, including sarcoma, represent tumours with rapid growth, accompanied by early formation of metastases.--In this connection all considerations concerning the usefulness of the so-called 'concept of pre-cancerosis' for the thyroid are thought to be very important. Realizing an atypical adenoma seems to be promising in evaluating this concept.
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PMID:[Malignant struma. With remarks on the use of the concept of precancerous conditions in strumas]. 652 26

A total of 18 nickel compounds were tested for carcinogenicity in male Fischer rats by a single i.m. injection at equivalent dosages (14 mg Ni/rat). Within two years, the following incidences of sarcomas occurred at the injection site: nickel subsulfide (alpha Ni3S2), 100%, crystalline nickel monosulfide (beta NiS), 100%; nickel ferrosulfide (Ni4FeS4), 100%; nickel oxide (NiO), 93%; nickel subselenide (Ni3Se2), 91%; nickel sulfarsenide (NiAsS), 88%; nickel disulfide (NiS2), 86%; nickel subarsenide (Ni5AS2), 85%; nickel dust, 65%; nickel antimonide (NiSb), 59%; nickel telluride (NiTe), 54%; nickel monoselenide (NiSe), 50%; nickel subarsenide (Ni11AS8), 50%; amorphous nickel monosulfide (NiS), 12%; nickel chromate (NiCrO4), 6%; nickel monoarsenide (NiAs), 0%; nickel titanate (NiTiO3), 0%, ferronickel alloy (NiFe1.6), 0%; 84 vehicle controls, 0%. Distant metastases were found in 109 of 180 sarcoma-bearing rats (61%). The nickel-induced sarcomas included rhabdomyosarcomas, 52%, fibrosarcomas, 18%, undifferentiated sarcomas, 13%, osteosarcomas, 8%, and miscellaneous and unclassified sarcomas, 9%. Kendall's rank-correlation test showed that the carcinogenic activities of the compounds were correlated (p = 0.02) with their nickel mass-fractions, but not with dissolution half-times in rat serum or renal cytosol, or with phagocytic indices by rat peritoneal macrophages in vitro. Rank-correlation (p less than 0.0001) was found between the carcinogenic activities and the potencies of the compounds to induce erythrocytosis in rats. The discovery that the carcinogenic activities of particulate nickel compounds are correlated with a physical property, namely the nickel mass-fraction, may help to elucidate the mechanisms of nickel carcinogenesis; the observation that nickel stimulation of erythropoiesis is correlated with carcinogenic activity provides a new in vivo screening test for use in determining the carcinogenic risk of nickel compounds.
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PMID:Carcinogenicity of nickel compounds in animals. 653 78

Pellets of 1 mg 9,10-dimethyl-1,3-benzanthracene (DMBA) were implanted into the submaxillary glands of 53 male C57BL/6J mice, and groups of mice were autopsied weekly or biweekly thereafter. Histologic evidence of tumor was noticed first at 12 weeks. From 16 weeks onwards, the submaxillary glands of all mice autopsied contained either carcinoma (three animals) or sarcoma (ten animals); 8/9 attempts to transplant these tumors in C57BL/6J mice were successful. Of the resulting eight tumor lines, two carcinomas and two fibrosarcomas were transplanted for over 30 months. Within the first few transplant generations, all four tumors showed an increase in growth rate and in histologic evidence of anaplasticity. For the particular tumors selected for study, the two carcinomas differed from the two sarcomas by growing more slowly, requiring more cells for tumor takes, and possessing a higher immunogenicity. These results may explain the types of tumors generated in submaxillary gland carcinogenesis. Carcinomas appear first, since they develop from the epithelial cells into which the carcinogen is implanted. Later, when fibroblasts wall off the carcinogen, fibroblasts are at risk for neoplastic conversion. Because of the more aggressive nature of the resultant fibrosarcoma cells, sarcomas may overgrow some early carcinomas.
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PMID:An explanation for the proportion of carcinomas and sarcomas seen in chemically induced murine submaxillary gland tumors. 680 25

The effects of manganese compounds upon the carcinogenicity of alpha Ni3S2 were tested in male Fischer rats. In Experiment I, rats were given i.m. injections of alpha Ni3S2 (2.5 mg) and Mn dust (2.0 mg), singly or in combination. By 100 weeks, sarcomas occurred at the injection site in 0 of 24 rats in the vehicle control group, in 0 of 24 rats that received Mn dust alone, and in 23 of 24 rats that received alpha Ni3S2 alone. Combined administration of alpha Ni3S2 plus Mn dust as a single i.m. injection resulted in sarcomas in 14 of 23 rats (p less than 0.05 versus alpha Ni3S2 alone). In rats that received injections of alpha Ni3S2 in one thigh and Mn dust in the opposite thigh, the sarcoma incidence at the site of alpha Ni3S2 injection was 24 of 24 rats. In Experiment II, rats were given i.m. injections of alpha Ni3S2 (1.2 mg) and Mn compounds (MnS, Mn2O3, MnO2 or MN2(CO)10, in dosages equivalent to 1.0 mg of Mn), singly or in combination. No sarcomas occurred at the injection site in rats that received the vehicle or any of the manganese compounds alone. Sarcomas occurred in 13 of 27 rats that received alpha Ni3S2 alone; this sarcoma incidence was not reduced by admixture of any of the Mn compounds. The median tumor latent period and the median survival period were significantly longer (p less than 0.05) in rats that received MnS plus alpha Ni3S2, compared with rats that received alpha Ni3S2 alone, suggesting that MnS may have weak anticarcinogenic effect. These experiments demonstrate that inhibition of alpha Ni3S2-carcinogenesis by Mn dust is a local rather than a systemic effect, and that, with the possible exception of MnS, the other manganese compounds that were tested are ineffective as inhibitors of alpha Ni3S2-carcinogenesis.
Carcinogenesis 1983
PMID:Effects of manganese compounds on carcinogenicity of nickel subsulfide in rats. 683 19

Several groups have shown that the malignant phenotype can be transferred to NIH/3T3 fibroblasts by incorporation of DNA isolated from tumour cell lines. These studies have demonstrated that the transforming activity of DNA isolated from human bladder, lung and colon carcinoma cell lines is related to an alteration of the cellular homologues of the ras genes of Harvey or Kirsten murine sarcoma viruses. It is, however, unclear what relevance these observations have to the multi-stage nature of tumorigenesis in vivo, in which several independent events are required in both humans and experimental animals. The activation of a cellular oncogene in a defined experimental system for the progressive induction of solid tumours has not yet been demonstrated. We report here that high molecular weight DNA from transplanted squamous cell carcinomas induced by sequential treatment of mouse skin with initiators and promoters of carcinogenesis causes morphological transformation of NIH/3T3 fibroblasts at high frequency. The transforming properties are due to the transfer of an activated cellular homologue of the Harvey-ras (rasH) oncogene.
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PMID:Mouse skin carcinomas induced in vivo by chemical carcinogens have a transforming Harvey-ras oncogene. 684 61

The established mouse cell line NIH 3T3 has been used with considerable success over the past three years as the basis of an in vitro transformation assay for demonstrating the presence of transfectable transforming genes in the DNA of certain human and rodent tumour cells (for review see ref. 1). In the case of the human bladder carcinoma cell lines EJ and T24, this approach has led to the molecular cloning of a transforming gene which is closely related to the rat-derived Harvey sarcoma virus oncogene, v-Ha-ras. A single point mutation, which distinguishes these genes from their normal human homologue (c-Ha-ras1), is thought to be solely responsible for their transforming potential. However, carcinogenesis in both humans and laboratory rodents is a multi-stage process (reviewed in ref. 11) of which the NIH 3T3 cell, already partly transformed, may represent only the penultimate stage. We therefore chose to examine the transforming effects of the EJ oncogene in a hamster fibroblast system originally developed in our laboratory to study stages in carcinogen-induced malignant transformation of normal diploid cells. We show here that EJ c-Ha-ras-1 lacks complete transforming activity when transfected into normal fibroblasts which have a limited lifespan, but can fully transform fibroblasts that have been newly 'immortalized' by carcinogens.
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PMID:Fibroblast immortality is a prerequisite for transformation by EJ c-Ha-ras oncogene. 687 85


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