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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pretreatment of chickens with BCG 1 week before inoculation with avian sarcoma virus had a stimulatory effect on virus-induced tumor growth in 15 of 17 cases tested. This outcome was dependent upon the injection of both BCG and the oncogenic agent into the same wing web. Injection of BCG into the wing web contralateral to that used for virus inoculation or injection of a subcellular fraction of BCG into the same wing web did not affect tumor development. Administration of BCG also gave rise to heightened levels of tumor-associated, cell-mediated immunity, both on the part of chickens which received a subsequent injection of oncogenic virus as well as normal, BCG-inoculated controls.
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PMID:Enhancement of avian sarcoma virus-induced tumor growth after pretreatment with BCG. 21 47

Rats were immunized with a single and repeated doses (1.0 mg of protein per dose per animal) of KCl-solubilized thymus and avian sarcoma virus B77-induced rat tumor cells LWF B77 prior to challenge with the same tumor cells. Results obtained showed that single administration of KCl-solubilized tumor cell material resulted in inhibition of growth of syngeneic tumor cells. Repeated inoculations of the same material, however, promoted tumor growth. Possible explanation of this dual effect is discussed.
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PMID:Inhibition and promotion of growth of B77-virus-induced rat tumor with KCl-solubilized tumor cell components. 22 46

Chick embryo (CE) fibroblasts and normal rat kidney (NRK) cells transformed by temperature-sensitive (ts) mutants of avian sarcoma virus (NY68, LA23, LA24, LA25, LA29, LA31, GI201, GI202, GI251, GI253 induce tumors on the chorioallantoic membrane (CAM) of chick eggs at temperatures that correspond to the permissive and nonpermissive temperatures used to induce conditional expression of the "transformed" phenotype in these cells when cultured in vitro. Chick embryo cells infected with transformation-defective mutants of ASV (td101, td108) or RAV-50 were nontumorigenic under the same conditions, as were nontransformed CE and NRK cells. This indicates that the CAM is not an unusually susceptible substrate for cell growth and that the ability of tsASV-transformed cells to form tumors at nonpermissive temperatures reflects their true tumorigenicity. In contrast, a ts mutant chemically transformed rat liver cell line, ts-223, only formed tumors on the CAM under permissive conditions. The wild-type parent cells (W-8) of this mutant produced tumors at both permissive and nonpermissive temperatures. Direct implantation of microprobe thermometers into tumors caused by ts-ASV-transformed cells at nonpermissive temperatures confirmed that tumor formation occurred in a stable temperature environment and was not due to temperature fluctuations which might have created semi-permissive conditions for tumor growth. Cells isolated from tumors formed at nonpermissive temperatures and recultured in vitro displayed temperature-dependent hexose transport and colony formation in agar similar to the orginal parent cell inoculum. Similarly, virus recovered from tumors at nonpermissive temperatures retained the ts mutation.
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PMID:Cells transformed by temperature-sensitive mutants of avian sarcoma virus cause tumors in vivo at permissive and nonpermissive temperatures. 22 65

Observations that the major histocompatibility (B) complex is a determinant of the growth pattern of Rous sarcoma virus (RSV)-induced tumors raised the question as to whether control is exerted at the level of a v-src-determined, i.e., transformation-specific, function. To investigate this point, the tumor size scores and tumor profile indices of v-src-induced tumors were compared in two lines of chickens congenic for B complex genotypes. The finding that the growth patterns of tumors, induced by v-src DNA inoculation at 6 weeks posthatch, differ in these two lines establishes that the B complex exerts control over tumor growth at the level of a v-src-determined function. The potential importance of this control, in terms of the naturally occurring case of an avian sarcoma virus infection, is suggested by the observation that the patterns of tumor growth in a given congenic line are similar whether the tumors are induced by v-src DNA or by RSV.
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PMID:Major histocompatibility (B) complex control of the growth pattern of v-src DNA-induced primary tumors. 132 33

Tumors which are induced in chickens by avian sarcoma virus frequently grow progressively for several weeks and then regress. We showed that tumor cells which are derived from the progressively growing phase of tumor growth produce large quantities of progeny-transforming virus, are reactive with antiviral antibody, and are susceptible to lysis in cell-mediated cytotoxicity assays by splenic lymphocytes of sensitized hosts. In contrast, tumor cells derived from regressing sarcomas are poor producers of progeny virus and are relatively unreactive with both antiviral antibody and sensitized lymphocytes. We further found that pp60src kinase activity was reduced by about 75% in regressing compared with progressively growing tumor cells. The half-lives of directly precipitable pp60src in tumor cells derived from progressively growing and regressing neoplasms were 6 and 1.5 h, respectively. Studies on each of three other cellular enzymes did not reveal any regression-associated decreases in enzyme activity. These data support the notion that expression of adequate levels of long-lived pp60src kinase activity is essential to progressive tumor growth.
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PMID:Immunological responsiveness against tumors induced by avian sarcoma virus: reduced expression of pp60src kinase activity in regressing tumors. 257 45

We have compared avian sarcoma cells, cultured from tumors at various stages of growth, in terms of their ability to synthesize infectious progeny virus and to express antigens that are reactive with the sensitized lymphocytes of tumor-bearing hosts. Cell-mediated immunity in chickens bearing tumors induced by avian sarcoma viruses was monitored by each of a target cell cytotoxicity test and an antigen-driven lymphocyte stimulation assay. Our results show that it is only those tumor cells which have been derived from progressively growing neoplasms that are able to synthesize infectious progeny virus and to specifically interact with the sensitized lymphocytes of tumor-bearing hosts. In contrast, cells from regressing tumors do not express relevant antigens to the same extent as do progressors, and they synthesize noninfectious particles only. Experiments on cellular outgrowths, derived from the plating at limited dilution of progressively growing tumor cells, revealed that such producers of defective virus are present at the earliest stages of tumor growth. Both these cells and regressing tumor cells are poorly stained (about 10%) in indirect immunofluorescence tests by antiserum against viral envelope glycoprotein, whereas tumor cells from progressing neoplasms react well (about 60 to 85%). These results suggest that tumor cells which are found in regressing neoplasms are selected out by a functional immune response directed against cells which are efficient producers of progeny virus.
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PMID:Immune selection of tumor cell variants in chickens bearing tumors induced by avian sarcoma virus. 627 81

Tumor cells which are cultured from the regressor phase of avian sarcoma virus (ASV)-induced tumor growth are deficient with respect to ability to produce progeny transforming virus. In addition, such cells are relatively unreactive with anti-viral antibody and are unable to elaborate, into the medium, antigens which are stimulatory to the sensitized lymphocytes of virus-injected hosts. These deficits can be overcome by treatment of the cells with the tumor promoter, phorbol myristate acetate (PMA).
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PMID:Alteration of phenotype of 'regressor' avian sarcoma cells following treatment with phorbol ester. 630 65