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

The long latent period required for tumor induction with Simian virus 40 (SV40) in the subcutis of hamsters can be used to investigate whether host factor(s) participate in oncogenesis. Several treatments were applied during this period, and the results were compared with those of the same treatment applied in another series of experiments, homologous SV40 tumor grafting in hamsters. The results obtained were as follows: (a) the latent period for SV40 tumor induction in the female was shorter than that in the male; tumor development was delayed significantly by oophorectomy but was little affected by orchiectomy. Tumor development was markedly delayed in animals of both sexes by estrone given at birth but was accelerated by testosterone given in the adult male; (b) by each of these hormonal modifications, growth of transplanted SV40 tumors was influenced in a different way from that of tumor induction; (c) immunosuppressive treatments, such as thymectomy, administration of antilymphocyte sera, cyclophosphamide, or cortisone acetate delayed and decreased tumor development when applied in the latent period, and the degree or pattern of this effect varied from one procedure to another, depending on the sex and age of the animals; (d) in contrast, tumor growth was markedly accelerated in thymectomized or cortisone-treated hosts irrespective of sex. The different and almost reverse effect of the same procedure in the two phases of tumorigenesis may indicate two discriminating mechanisms operating in the host during these phases. This different effect may be due to virtual absence of any "mature" neoplastic cell in the latent period, except for a few weeks before the appearance of a palpable tumor. These results suggest that the long period of latency may be spent to complete SV40-induced neoplastic conversion of cells, receiving some help by host factors.
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PMID:Suppressive effects on simian virus 40-induced oncogenesis of several immunosuppressive agents and hormonal modifications applied during the latent period. 21 31

Simian virus 40 (SV40), a DNA-containing tumor virus in the papovavirus group, represents an ideal model system for the analysis of the mechanism of viral-induced tumorigenesis because of the small size of its genome and its broad range of oncogenic potential. Viral genes persist and are expressed in SV40-transformed cells. Temperature-sensitive (ts) mutants of the virus have proved to be valuable tools for the identification and analysis of viral gene expression in transformed cells. Through the use of such mutants, it has been determined that a specific gene product (A-protein) is required to initiate cellular transformation. The role of virus genes in the maintenance of the transformed state was determined by transformation of the cells of mouse, hamster, and human origin by ts virus containing A-gene mutations. These cells were then examined under permissive and nonpermissive conditions for the presence of a variety of intracellular and surface alterations commonly associated with neoplastic transformation. From the results of such experiments, it has been concluded that an SV40-specific function is also necessary for the maintenance of at least some of the phenotypic properties of the transformed state. Indirect evidence, derived from a comparison of the biological and biochemical properties of the SV40-induced tumor (T) antigen and the gene A-protein, supports the idea that T-antigen is a product of the A-gene. One model devised to explain the mechanism by which the gene A-protein might function as an effector of transformation is presented.
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PMID:Transformation by viruses: simian virus 40 as a model system. 21 55

The potent tumor promoter, 12-O-tetradecanoylphorbol-13-acetate, produced a 2- to 3-fold increase in the activity of both the low- and high-affinity forms of cyclic adenosine 3':5'-monophosphate phosphodiesterase activity 13 hr after application to mouse skin. The magnitude of the enzyme induction correlated with the tumor-promoting activity of several doses of 12-O-tetradecanoylphorbol-13-acetate and of other phorbol esters. The induction of the low-affinity phosphodiesterase could be blocked by prior i.p. injection of the microtubule poisons, colchicine and vinblastine. The low-affinity cyclic adenosine 3':5'-monophosphate phosphodiesterase activity of the epidermal component of mouse skin papillomas produced by two-stage tumorigenesis was 3 times that of the surrounding uninvolved epidermis.
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PMID:Increased cyclic adenosine 3':5'-monophosphate phosphodiesterase activity in the epidermis of phorbol ester-treated mouse skin and in papillomas. 22 Oct 99

Macrophages form S- and K-strain Leghorn chickens, susceptible and restant to Marek's disease (MD) respectively, were studied to determine the macrophage contribution to the dynamics of MD infection, tumorigenesis and genetic resistance to this disease. In vitro studies demonstrated that macrophages from bothstrains were similar in their responses toward JM strain of Marek's disease virus (MDV) and JM-1 tumor cells. Macrophages were observed to phagocytize JM virus, but the interiorized virus was not seen to replicate within the macrophage or induce antigenic changes of the cell membrane. Clearance of JM-1 tumor cells was by both cytolytic and phagocytic mechanism. In vivo selective suppression of macrophage functions by antimacrophage serum or trypan blue inoculations resulted in significantly elevated viral titers and increased tumorigenesis, as compared to infected, non-suppressed or non-infected control groups. Results from this study indicate that genetic susceptibility or resistance to MD, as exhibited by S- and K-strain chickens, respectively, is not controlled at the macrophage level. The role of the macrophage in MD infection appears to be specifically surveillance.
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PMID:The role of the macrophages in Marek's disease: in vitro and in vivo studies. 22 92

The tumorigenicity of DNA from polyoma virus after cleavage with a variety of restriction enzymes was evaluated in suckling hamsters. Cleavage with enzymes that interrupt the region of the genome coding for the large tumor (T) antigen of polyoma virus markedly enhanced the tumorigenicity above that observed with DNA I of the virus. Cell lines established in vitro from tumors induced by polyoma virions, polyoma virus DNA I, or polyoma virus DNA that had been cleaved with restriction endonucleases in the early region all contain the polyoma virus middle and small T antigens but not the large T antigen of polyoma virus is not required for maintenance of the transformed state and probably not for initiation of tumorigenesis by viral DNA.
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PMID:Interrupting the early region of polyoma virus DNA enhances tumorigenicity. 22 75

As part of the national survey on the tumorigenesis of oral contraceptive drugs conducted by the American College of Surgeons' Commission on Cancer, a histologic study was made of 94 cases of liver tumors in users and non-users of oral contraceptives. Pathologic criteria were established and then the slides were studied; the results were tabulated to determine the significance of each of the criteria as related to the use of contraceptives. These criteria included tumor size, peliosis hepatis, hemorrhage, necrosis, fibrosis, thrombosis, and vascular alterations of the intima and media. Cases of focal nodular hyperplasia in pill users exhibited greater vascular alterations, fibrosis, peliosis, and tumor size as compared to focal nodular hyperplasia observed in non-pill users. In addition, hemorrhage, necrosis, and peliosis were much more common in hepatic cell adenoma than in focal nodular hyperplasia. In the material reported in this series there were no hepatic cell adenoma cases observed in non-pill users. Focal nodular hyperplasia cases exhibited an overwhelmingly greater degree of vascular intimal and medial alterations than hepatic cell adenoma. The results suggest that the effects of oral contraceptives on the liver may be primarily upon the vasculature.
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PMID:The histology of liver tumors in oral contraceptive users observed during a national survey by the American College of Surgeons Commission on Cancer. 22 66

Prolactin receptors have been identified for the first time in a number of human breast cancer cell lines and a normal human breast cell line maintained in long-term tissue culture. Optimal conditions for determining the binding of 125I-labeled human prolactin to these cells were established. Five different tumor cell lines have different content of prolactin receptors ranging from 2,300 to 26,000 sites/cell. All tumor cell lines contained more prolactin receptors than does one normal breast cell line (1700 sites/cell). The prolactin receptors in these human mammary tumor cells not only bind human prolactin but also recognize other lactogenic hormones such as human growth hormone, human placental lactogen, and sheep prolactin, but not animal growth hormone, which are not lactogenic. The affinity (Ka) of binding of human prolactin to these cells is 4 x 10(9) M-1 (Kd = 2.5 x 10(-10)M). The hormone specificity and affinity for hormone of these human mammary tumor cells are very similar to that found for the rabbit mammary gland. These human mammary tumor cell lines in long-term culture should prove very useful to study the biology of prolactin receptors in living human cells and the role of prolactin in the tumorigenesis of the human breast.
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PMID:Prolactin receptors in human breast cancer cells in long-term tissue culture. 22 85

Involvement of mouse mammary tumor virus (MMTV) in 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary tumorigenesis was investigated in low- (BALB/c) and high- (BALB/cfC3H) mammary-tumor-incidence mouse strains. Both strains contain endogenous MMTV integrated into the cellular genome. Additionally, BALB/cfC3H mice are infected with exogenous MMTV-S which is responsible for a higher incidence of mammary tumors in breeding females. Administration of DMBA to virgin mice of both strains resulted in a moderate frequency of mammary tumors within 40 wk after treatment. No differences were found in DMBA-induced tumor incidences at 18 wk (6% and 7%) or at 38 wk (29% and 36%) after treatment of BALB/c and BALB/cfC3H mice, respectively. Expression of MMTV in these tumors was examined by assaying for the presence of MMTV RNA by hybridization using MMTV-specific cDNA and by immunohistochemical staining utilizing antibodies against MMTV 52,000-dalton glycoprotein, gp52, and 28,000-dalton internal protein, p28. Of 16 BALB/c tumors assayed, 11 did not contain detectable levels of MMTV RNA and the remaining 5 tumors contained only low levels (0.0005-0.0010%) of viral RNA. Importantly, MMTV RNA was not detected in 5 of 27 BALB/cfC3H tumors. The other BALB/cfC3H tumors contained quantities of MMTV RNA ranging from 0.0006 to 0.4170%. Most BALB/cfC3H tumors with detectable levels of MMTV RNA also synthesized viral proteins gp52 and p28. Thus, expression of the complete MMTV genome is not requisite for maintenance of the tumor phenotype in DMBA-induced mammary tumors in either BALB/c or BALB/cfC3H virgin mice under 1 year of age.
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PMID:Mouse mammary tumor virus genome expression in chemical carcinogen-induced mammary tumors in low- and high-tumor-incidence mouse strains. 22 89

The in vitro effects of asbestos fibers on the growth and viability of CHO cells, an epithelioid cell line derived from Chinese hamster ovary, and on K-22 cells, an epithelial cell line derived from rat liver, have been studied. Relatively low concentrations of asbestos (10 micrograms/ml) were quite cytotoxic to both cell types. A sample of chrysotile asbestos was more toxic than samples of crocidolite or amosite. The toxic factor could not be extracted from the asbestos and toxicity occurred only if there was physical contact between the fibers and the cells. Although the phorbol ester class of tumor promoters induces the synthesis of plasminogen activator in various cell cultures, asbestos did not induce this protease in epithelioid or fibroblast cell cultures. The results obtained are compared to previous in vitro results obtained with fibroblast or macrophage cultures and are discussed in terms of their possible relevance to asbestos-induced fibrosis and tumorigenesis.
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PMID:Effects of asbestos on epithelioid cell lines. 23 16

Histophysiology, ultrastructure, chemical analyses of transplants and implants of Dunn and Ridgway mouse osteosarcomas demonstrate that tumorigenesis is a manifestation of deranged morphogenesis in developing mesenchymal cell populations. The end product of development is defective, incompletely calcified, disorganized bone without any inclusions of bone marrow tissue. When Dunn osteosarcoma is freeze-dried and then implanted, the tumor is resorbed and replaced by deposits of normal cartilage, bone, and bone marrow. Freeze-dried Ridgway osteosarcoma is replaced only by a fibrous connective tissue scar. Disaggregated Dunn tumor osteoblasts synthesize a trypsin-labile collagenase-resistant cell surface localized bone morphogen. Tumor matrix stroma, prepared by sequential chemical extraction of soluble non-collagenous proteins also contains significant quantities of the same bone morphogen. Tumor tissue pulverized to particle size as small as 44 micrometer3 transmitted bone morphogen more rapidly than intact tumor tissue. The total tumor cell and stroma mediated bone morphogen produces three times more normal bone than normal cortical bone matrix. Our working hypothesis is that a normal bone morphogenetic polypeptide (BMP) is synthesized by Dunn osteosarcoma cells and retained by the tumor matrix stroma. Neither the mechanism of transmission nor the mesenchymal cell receptor sites of BMP are known.
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PMID:An osteosarcoma cell and matrix retained morphogen for normal bone formation. 27 29


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