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

This brief review paper deals mainly with oncogenic DNA viruses originally isolated from human patients, i.e., human adenoviruses and human papova JC viruses. Human adenovirus type 12 was first isolated in 1953 in cell cultures derived from the adenoids of infected children. Since then, 32 antigenic types of human adenovirus have been identified. At least eight serotypes (12, 18, 31, 3, 7, 14, 16, and 21) are now known to be capable of producing tumors in newborn rodents. A direct causal relationship between a human adenovirus and malignant transformations in target cells (sensory neuronal precursors) has been definitely established by the development of a medullo-epitheliomatous neoplasm in the brain and spinal cord of an outbred strain of CD rats at as high an incidence as 90%. Intraocular inoculation of adenovirus in newborn rats within one week also has produced typical retinoblastomatous neoplasms. The remarkably uniform histopathologic appearance of all these malignancies in nervous tissue can be attributed to a primitive neuro-epitheliomatous neoplasm derived from sensory microneuron precursors that densely populate both the ventricular zone and the premature sensory retina at the point of virus inoculation. All of these brain and retinal tumors appear to share a common tumor phenotype, as all tumor cells contain cilia with the same morphology (a 9+0 pattern of doublets associated with a pair of centrioles). The production of adenovirus tumor-specific neoantigen (T), an earmark of the viral genome, can be regularly demonstrated by the immunofluorescein microscopic procedure. All transformed cells within both the ventricular zone and the retinal ganglion cell anlage thus appear to continue the production of (T) antigens. These findings lead us to assume that the target cell determinants in adenovirus tumorigenesis may reside in differentiating microneuron precursors ordained for the sensory neuronal complex.
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PMID:[Viruses and brain tumors (author's transl)]. 17 19

High doses of vitamin A decreased the severity of tumor development in mice inoculated with a murine sarcoma virus; the same doses of vitamin A had no effect on the increased tumorigenesis seen in animals severely stressed with thermal injury or the increased tumorigenesis induced by exogenous glucocorticoid administration.
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PMID:Effect of vitamin A on tumor development in burned, unburned, and glucocorticoid-treated mice inoculated with an oncogenic virus. 17 74

The inoculation of Polyoma virus suspension to neonatal pinealectomized rats did not provoke a growth of neoplasia. However, if the pinealectomy was combined with neonatal thymectomy, renal tumors occured in a rate of 50 of animals. An incidence of renal tumors was observed also in 57.6% of thymectomized rats, but not in non operated control group. The stimulating effect of pinealectomy on the growth of transplantable tumors has already been described several times (2, 3, 6, 8). The question of a possible change in the viral oncogenesis after pinealectomy was raised. For this reason Polyoma virus was used and its oncogenic effect was studied on the neonatally pinealectomized rats, on rats neonatally thymectomized and on neonatally pinealectomized rats which were simultaneously thymectomized.
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PMID:The influence of pinealectomy and of pinealectomy combined with thymectomy oncogenesis caused by polyoma virus in rats. 17 46

A single i.m. dose of formalin-inactivated murine mammary tumor virus greatly reduces viral expression and mammary tumorigenesis in Af (tumor incidence, 39%) and RIIIf (tumor incidence, 11%) mice, which carry only endogenous, gamete-transmitted virus. In C57BL mice, 1 mug of vaccine in Freund's complete adjuvant protects against later challenge with RIII virus.
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PMID:Further immunization studies with mammary tumor virus. 17 38

To study the function of different lymphocyte populations in the Moloney strain of murine sarcoma virus (M-MuSV) tumorigenesis, we gave M-MuSV injections to CBA mice selectively deprived of thymus (T) lymphocytes by thymectomy, X-rradiation, and syngeneic bone marrow injection. Although no tumors appeared in the control group, 80% of the derived mice had tumors that grew progressively and ultimately killed them. In deprived mice, grafted with a syngeneic thymus (reconstituted mice) before or after an M-MuSV injection, tumors regressed or did not develop. Histologically, the lymph nodes and spleens of reconstituted mice, compared to those of deprived animals, showed repopulation of the thymus-dependent areas and prominent follicles in the cortex. Moreover, tumor tissue of reconstituted mice was extensively infiltrated by lymphocytes. To evaluate the number of lymphoid cells needed to prevent or regress M-MuSV tumors, we injected varying amounts of lymphoid cells into deprived mice. Even low lymphocyte numbers (10(6) cells) were sufficient to exert, in some cases, protection against M-MuSV tumorigenesis. This effect was not abolished by subsequent splenectomy or antilymphocyte serum treatment. Finally, deprived mice, given repeated injections of antiserum (hyperimmune) against M-MuSV, had tumors which appeared only after a prolonged latency. From these results, it is concluded that T-cell population integrity is important in affording total host protection against the M-MuSV tumors.
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PMID:Immune reactivity in the Moloney strain of murine sarcoma virus oncogenesis: requirement of thymus-derived lymphocytes for in vivo protection. 17 99

A total 39 kidney tumors were induced by a continuous oral administration of N-butylnitrosourea (BNU) in 33 out of 204 rats of W/Fu strain and of 41 (W/Fu X ACI/N)F1 rats. No spontaneous renal tumors were observed among 66 males and 109 females of W/Fu rats which survived beyond the age of 19 months. Histologically, renal cell and mesenchymal types were commonly observed; 24 cases belonging to the former and 11 cases to the latter. Two cases of nephroblastoma were also encountered. There was no sex difference in renal tumorigenesis with BNU as a whole. Castration in both sexes was apparently inhibitory for kidney tumor development. Estrogenization of castrated rats either by syngeneic ovary graft or by repeated injections of estradiol benzoate enhanced tumor induction with BNU. Progesterone was not effective in restoring the tumor incidence in castrated rats. Distribution of histological types of tumors thus induced differed among the hosts with different hormonal conditions; in males the majority was renal cell type, whereas almost all mesenchymal tumor and nephroblastoma cases were found in intact females or estrogenized rats. BNU induced a variety of tumors in several organs including cerebral hemisphere, peripheral nerves, mammary glands, hematopoietic system, digestive tracts, and so on. However, such concurrence did not affect the development of renal tumors in the present study.
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PMID:Influence of sex hormones on kidney tumors induced in rats with N-butylnitrosourea. 17 65

AKR mice produce, from shortly after birth, high titers of their endogenous Gross type murine leukemia virus, and develop a thymus-derived leukemia at 7-9 months of age. We show that this oncogenesis is accompanied by an increase in the number of AKR-specific DNA sequences in the tumor tissues, whereas the "non-target" organs are not affected. Sequence increase was determined by kinetic analysis of DNA reassociation using an AKR-murine leukemia virus (MuLV)-specific cDNA and also by hybridization with excess AKR cDNA. The AKR cDNA was selected to recognize AKR sequences without significant crossreaction with DNA sequences of other endogenous viruses. The results show that during the development of the leukemia, the number of AKR-MuLV-specific genes increases in tumor tissues by a factor of 1 1/2 to 2.
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PMID:Increase of AKR-specific sequences in tumor tissues of leukemic AKR mice. 18 52

Case reports of neuroblastoma revealed that some individuals are genetically predisposed and that this genetic predisposition may have other consequences. According to a mutation model, two classes of individuals could acquire neuroblastoma. One (prezygotic) was a rare class that carried a dominant gene imparting high risk of the tumor. The other (postzygotic) comprised all other individuals, each at low risk. The model related tumor incidence to germinal and somatic mutation rates and thereby carried implications for environmental modification of tumorigenesis and demographic variation in incidence. Case reports also revealed associations of neuroblastoma with congenital defects and a susceptibility to second tumors. Analogy with retinoblastoma and Wilms' tumor of the kidney suggested that these associations could result from action of a neuroblastoma gene or from chromosomal aberration. One known dominantly inherited condition, von Recklinghausen's disease, could dispose to neuroblastoma and create some associations. According to the two-mutation model, neuroblastoma may have been a single recessive gene disorder at the level of the cell. The phenomena of aganglionosis, neuroblastoma in situ, maturation of neuroblastoma to ganglioneuroma, and spontaneous regression suggested that such a neuroblastoma gene interfered with normal developmental processes. The specificities of this gene and of those for von Recklinghausen's disease and pheochromocytoma suggested that the functiof a membrane macromolecule.
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PMID:Developmental genetics of neuroblastoma. 18 2

When BALB/cfC3H females are subjected to continous suction thymectomy, a procedure that results in retention of thymic remnants, the latent period before tumor development is significantly prolonged. However, when BALB/cfC3H females are thymectomized by control suction, a procedure which removes thymic lobes completely, there is no effect on mammary tumorigenesis. Our results show that incomplete T cell depletion causes premature onset of non-T cell cytotoxicity, an augmentation of T cell cytotoxicity, and an alteration in a serum-blocking activity to mammary tumor target cells as tested in microcytotoxicity assay. On the other hand, complete neonatal thymectomy effectively and completely abrogates immune response to mammary tumor target cells. The inability of completely thymectomized mice to generate an immune response to MTV suggests (but does not prove) that MTV-induced mammary tumor target cell surface antigens are thymus-dependent.
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PMID:Stimulation of immune mechanisms against mammary tumors by incomplete T cell depletion. 18 35

C3H/HeJ and AKR/J mice differed in their susceptibility to 3-methylcholantrhene (MCA)-induced sarcomagenesis (86% incidence of sarcomas in C3H by 18 wk; 5% incidence in AKR by 18 wk) and in the production of endogenous murine leukemia virus (MuLV) (AKR produced greater than 10(5) plaque-forming units/ml tail extract in XC test; C3H did not produce detectable virus.) A genetic corss between C3H and AKR mice was examined to determine the relationship of virus production to oncogenesis by MCA. Mice of the (C3H X AKR)F X C3H backcross were typed for the production of infectious MuLV by tail biospy and then inoculated with MCA. Of the backcross mice, 81% produced high titers of ecotropic MuLV; the remaining 19% did not contain detectable infectious MuLV. The virus-producing and non-virus-producing backcross mice were equally sensitive and highly susceptible to MCA-induced sarcomagenesis. Tumors of all virus-positive mice contained infectious MuLV. Some tumors (54%) of virus-negative mice also contained infectious MuLV; this indicated the induction of endogenous MuLV in the tumors of these mice. We concluded that the overt production of MuLV in mice of this backcross did not function in the sensitivity of the mice to sarcoma induction by MCA. Furthermore, the presence of virus in some chemically induced tumors was due to an induction pehnomenon independent of the primary oncogenic event.
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PMID:Endogenous oncornaviruses in chemically induced transformation. II. Effect of virus production in vivo. 18 3


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