Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Avian-leukosis-free females from Regional Poultry Research Laboratory (RPRL) inbred lines 6(1) and 7(2) were inseminated with pooled semen from RPRL line 15I5 males. The progeny resulting from the two crosses 15I5 X 6(1) and 15I5 X 7(2) were of the B2/B15 major histocompatibility complex (MHC) genotype, the B2 haplotypes from lines 6(1) and 7(2) being indistinguishable. When challenged with Rous sarcoma virus (RSV) at 6 weeks of age, 30 out of 31 progeny of cross 15I5 X 6(1) developed tumors that rapidly regressed, whereas 26 of 29 progeny of cross 15I5 X 7(2) died with progressive tumor growth. On the other hand, 15 of 18 B2/B15 segregants from the three-way cross (15I5 X 6(3]F1 X 7(2), identical in source to the MHC of the (15I5 X 7(2]F1 progressors, were characterized by tumor regression. Thus influences associated with non-MHC background genes from lines 6(1), 6(3), and 7(2) appeared to be critical to host response to RSV-induced sarcomas. Similar findings suggesting a strong non-MHC influence on anti-sarcoma response were obtained using 107 F2 and 77 backcross progeny of RPRL line 100 and noninbred University of New Hampshire (UNH) line 105. The B2 haplotype of line 100 was associated with tumor regression when combined with the line 105 background and with tumor progression when expressed on the line 100 background. Suppression of the anti-tumor response associated with line 100 appeared to be fairly generalized, since a poor response to tumor was observed regardless of which of three subgroups of RSV was used to induce tumor.
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PMID:A non-MHC genetic influence on response to Rous sarcoma virus-induced tumors in chickens. 609 53

The Carr-Zilber strain of Rous sarcoma virus is highly oncogenic for adult monkeys of the species Macaca mulata. In the present study, we examined some characteristics of tumor growth when the tumor either regressed or progressed until it killed its host. We followed the kinetics of antibody formation to antigens coded by CZ-RSV in animals with a different course of tumor disease. The sera of animals tested contained virus-neutralizing antibodies, in addition to gs antibodies. The results are discussed with regard to the possible virus-productive type of interaction between RSV and the monkey cell.
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PMID:Characterization of tumors induced in adult Macaca mulata monkeys with Carr-Zilber strain of Rous sarcoma virus. 624

The Carr-Zilber strain of Rous sarcoma virus is highly oncogenic for adult monkeys of the species Macaca mulata. In the present study the authors examined some characteristics of tumor growth, when the tumor either regressed or progressed until it killed its host. The kinetics of antibody formation to antigens coded as CZ-RSV was followed in animals with a different course of tumor disease. The sera of animals under test contained virus-neutralizing antibodies in addition to gs antibodies.
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PMID:[Rous virus-induced sarcoma study of Macaca mulatta monkeys]. 625 76

In Japanese quails treated with chicken amniotic fluid (ChAmF) which had been previously shown to induce suppressor cells to natural killer (NK) cells, tumors appeared with shortened incubation periods after inoculation with Schmidt-Ruppin strain of Rous sarcoma virus (SR-RSV) compared with untreated quails. The tumors in ChAmF-treated quails subsequently grew in a similar pattern to those in untreated quails, whereas by challenging with a lower dose of the virus, enhanced tumor growth was observed as well as earlier onset of tumors in ChAmF-treated quails than in untreated ones. This enhancing effect on tumor growth due to suppression of NK-cell activity was transferred to normal quails with spleen cells obtained from ChAmF-treated quails, since RSV-induced tumors appeared earlier in the recipients of ChAmF-treated spleen cells than in those of untreated spleen cells. These findings show that suppression of NK-cell activity by ChAmF administration rendered quails higher susceptibility to tumor induction by SR-RSV challenge. In other words, NK-cell activity was strongly suggested to contribute to the early protection against tumor growth in the system of Rous sarcoma in Japanese quails.
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PMID:The role of NK cells in tumor growth assessed by induction of their suppressor cells in Japanese quails. 627 20

The inhibitory effect on tumor growth of thymus-derived cells in the avian virus system has been demonstrated by several investigators. Here we report two kinds of experiments performed to test the role of various potential effector cells in the immune response against Rous sarcomas. In vivo experiments in Japanese quail using the antimacrophage agent silica implicate the macrophage as a further mechanism in the defense against Rous sarcoma virus-induced tumors. Induction of a nonspecific inflammation at the site of tumor development led to reduced tumor growth.
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PMID:Effector mechanisms against Rous sarcomas in quail. 630 87

The anti-sarcoma response of three B complex recombinant haplotypes BR1(F24-G23), BR2(F2-G23), and BR3(F2-G23) was investigated. In a preliminary experiment, one male heterozygous for the BR1 recombinant haplotype and another heterozygous for the BR2 recombinant haplotype were each mated to females, some of which carried the respective recombinant. The anti-sarcoma response of progeny carrying the BR1 recombinant differed significantly from that of progeny carrying the BR2 recombinant. Subsequently, each of the three recombinant haplotypes was placed on each of four B haplotype complex backgrounds, and compared to B-G and B-L/B-F region controls on the same background haplotype. For each recombinant, significant differences in tumor growth were found between the recombinant and B-L/B-F control chickens on either one, two, or three of the four genetic backgrounds tested. For each recombinant, no differences were found between chickens carrying the recombinant and B-G region controls, which is further evidence that the gene(s) controlling Rous sarcoma growth lies in or near the B-L/B-F chromosomal region. Moreover, although the BR2 and BR3 recombinants appear to be identical serologically, they differed significantly in tumor growth suggesting that the two haplotypes are genetically different.
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PMID:B-complex recombinants and sarcoma regression: role of B-L/B-F region genes. 776 28

In male Japanese quail, different circulating leukocyte responses were observed for progressors (birds developing a massive tumor that persisted throughout the experiment) and regressors (birds developing a tumor that gradually disappeared) after initial challenge with Rous sarcoma virus (RSV). Blood was sampled before and at weekly intervals postinoculation. Blood smears were prepared and stained with Diff Quik, and a light microscope (1000 x) was used in a direct count of 50 fields. Leukocytes were classified as heterophils, lymphocytes, monocytes, or eosinophils. The significant increase (P < 0.05) in total leukocytes at 14 days in regressors and progressors was consistent with the increase in tumor growth. The regressors' individual percentage of leukocytes did not deviate from control values, whereas the progressors' percentages of heterophils and monocytes were significantly higher (P < 0.05) and of lymphocytes significantly lower (P < 0.05) than those of controls by 14 days postinoculation. Indicative of this was the progressors' heterophil to lymphocyte ratio, which was significantly higher (P < 0.05) than that of controls 14 days post RSV challenge and remained elevated throughout the experiment. These findings suggest that the progressors' immune response is suppressed by proliferation of malignant cells. Therefore, the heterophil to lymphocyte ratio may be used in addition to tumor size to identify those birds that will regress RSV-induced tumors.
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PMID:The leukocyte response of Japanese quail to Rous sarcoma virus-induced tumors. 783 16

The concentration of serum C3 in quails bearing tumors induced by Rous sarcoma virus (RSV) was elevated in parallel with tumor growth, whereas serum C3 levels in quails inoculated with avian leukosis virus, which lacks transforming activity, showed a pattern similar to that in mock-infected quails. C3 deposition was also observed in almost all tumor cells at the tumor developing stage. These findings obtained in vivo suggest that the cells transformed by RSV activated the C3 on their surfaces.
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PMID:Activation of complement in quails bearing Rous sarcoma virus-induced tumors. 872 51

Type I interferons have potent antiproliferative activity both in vitro and in vivo, and their tumor suppressor activity has been suggested. A series of eukaryotic vectors containing a synthetic human consensus type I interferon gene (IFN-con1) under the control of different promoters (cytomegalovirus early promoter, murine metallothionein promoter and the Rous sarcoma virus LTR) were constructed and stably transfected into type I IFN-deficient myelogenous leukemic K562 cells. Constitutive expression of IFNcon1 reverted the malignant phenotype, as indicated by loss of tumorgenicity in nude mice. When stably transformed cells were mixed with parental tumor cells, there was retardation of tumor growth. Constitutive expression of IFNcon1 reverted the malignant phenotype in vitro, as indicated by growth inhibition in culture, and reduction in colony formation on soft agar. Furthermore, IFNcon1 gene expression resulted in elevated erythroid differentiation, growth arrest in S phase and induced apoptosis. Thus the presence of an active IFNcon1 gene overcomes the oncogenic potential of K562 by coordinated modulation of cell proliferation, differentiation and programmed cell death, and it acts as a tumor suppressor in vivo.
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PMID:Tumor suppressor activity of the human consensus type I interferon gene. 938 82

Our laboratory has developed two cellular models of human prostate cancer progression. The LNCaP prostate cancer progression model is based upon the well-known cellular interaction between human prostate or bone stromal cells and LNCaP cells in vivo. The marginally tumorigenic LNCaP cells acquired tumorigenic and metastatic potential upon cellular interaction with either prostate or bone fibroblasts. A subline termed C4-2 was observed to grow readily in castrated animals and acquired metastatic potential spreading from the primary tumor site to the lymph node, the seminal vesicles, and the axial skeleton, resulting in an intense osteoblastic reaction. The second model is ARCaP, where prostate cancer cells derived from the ascites fluid of a man with metastatic disease exhibited an Androgen- and estrogen-Repressed Prostate Cancer cell growth and tumor formation in either a hormone-deficient or a castrated environment. However, the growth of either the tumor cells in vitro or the tumors in vivo was suppressed by both estrogen and androgen. While the tumor cells expressed low levels of androgen receptor and prostate-specific antigen (PSA), they were highly metastatic when inoculated orthotopically. Distant metastases to a number of organs were detected, including the liver, lung, kidney, and bone. We have employed a human prostate cancer progression model as a system to study the efficacy of gene therapy. Results of the study show that whereas universal promoters, such as Cytomegalovirus (CMV) and Rous Sarcoma Virus (RSV) promoter-driven tumor suppressors (e.g. p53, p21, and p16), were effective in inhibiting prostate tumor growth, the advantages of driving the expression of therapeutic toxic genes using a tissue-specific promoter prostate-specific antigen (PSA) and a tumor--but not tissue-specific promoter, osteocalcin (OC), are preferred. In the case of the PSA promoter, we can achieve cell-kill in PSA-producing human prostate cancer cells. To circumvent the supporting role of bone stroma for prostate cancer epithelial growth, we have recently developed a novel concept where the expression of therapeutic toxic genes is driven by a tumor--but not a tissue-specific OC promoter. Osteocalcin-thymidine kinase (OC-TK) was found to efficiently eradicate the growth of osteosarcoma, prostate, and brain tumors both in vitro and in vivo. We observed that androgen-independent human prostate cancer cells lines expressed OC-TK at higher levels than androgen-dependent human prostate cancer cell lines. We have obtained data to suggest that Ad-OC-TK plus a pro-drug acyclovir (ACV) may be used as an effective therapy to treat prostate cancer bone metastasis in models where the growth of androgen-independent PC-3 and C4-2 tumors in the bone has occurred.
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PMID:Human prostate cancer progression models and therapeutic intervention. 943 28


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