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

Reserach was conducted to determine whether development and subsequent regression of a Rous sarcoma virus (RSV) induced wing-web tumor influenced egg production. Fifty-seven six-week old pullet chicks of inbred line 6 of the United States Department of Agriculture, Regional Poultry Research Laboratory, East Lansing, Michigan, were inoculated subcutaneously in the left wing-web with 0.1 ml. of a 10-minus 3 dilution of a pseudotype of Bryan high titer RSV designated BH-RSV (RAV-1). Thirty chicks were left uninoculated. Each chick was examined for tumor growth at regular intervals to 10 weeks post-inoculation. A tumor was considered regressed if it disappeared completely. Ninteen regressor and 22 uninoculated females were placed in laying cages at 4.5 months of age and egg production data obtained over seven 28-day periods. The difference in hen-day egg production between regressors and uninoculated controls favored regressors by 2.7 eggs/bird and was statistically significant. Physiological stimulus from cellular immunity, linkage and pleiotropy are discussed as possible caused of the higher egg production in regressors.
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PMID:Effect of regression of Rous sarcoma tumors upon egg production in an inbred line of White Leghorns. 16 64

Temporal appearance of cellular cytotoxicity and humoral activities including blocking and arming activities during the entire course of Rous sarcoma development in Japanese quails was examined by microcytotoxicity assay with comparison of animals bearing regressing tumors induced by a moderate dose of virus (regressors) and animals bearing growing tumors induced by a large dose of virus (progressors). Cellular cytotoxicity of the spleen cells in regressors was detected in a biphasic pattern; the first phase being observed as early as 3-5 days post inoculation (p.i.), followed by an eclipse period between 7-10 days p.i. which was the time of active tumor growth, and the second phase occurring after 12 days p.i. when the tumor had attained the maximum size. In progressors, only the first phase was observed. Instead, a stimulatory effect of the spleen cells on growth of target cells was noticed. Arming activity which confers cytotoxic activity on the normal spleen cells was demonstrated in the sera of regressors in the similar biphasic pattern as the cellular cytotoxicity; the early activity being present at 3 days p.i., and the late one after 19 days p.i. The former was detected by pre-incubation of serum with effector cells in microcytotoxicity assay and the latter by pre-incubation with target cells. In progressors, only the early arming activity which reacts with effector cells was demonstrated. Blocking activity which abrogates cellular cytotoxicity was demonstrated in both regressors and progressors but in different patterns of appearance, that is, blocking activity in regressors was only transiently demonstrated only by pre-incubation with effector cells at the time of maximum tumor growth, while the activity in progressors seemed to persist after the tumor reached the maximum size. Since the earlier activity was found to be effective at effector cell level, and the later one at both effector and target cell levels, participation of blocking factors of different types in progressors was also suggested.
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PMID:Temporal analysis of cellular cytotoxicity and humoral factors during progession and regression of Rous sarcomas in Japanese quails. 18 34

The effect of inoculating formalinized syngeneic or allogeneic Rous sarcoma cells on the growth of Rous sarcoma virus (RSV)-induced tumors in two related inbred strains of chickens was studied. Chickens from both strains that received three weakly inoculations of syngeneic tumor cells had a significant increase in tumor growth and mortality after subsequent challenge with RSV. Development of RSV-induced tumors in chickens pretreated with formalinized allogeneic tumor cells (i.e. incompatible for major histocompatibility complex (MHC) antigens) was similar to what we observed in nonpretreated control chickens. The finding that the tumor-host relationship is altered only in chickens pretreated with formalinized syngeneic RSV-transformed cells, suggests that tumor-associated antigens of Rous sarcomas are modified MHC antigens analogous to "altered self" antigens thought to be present on certain virus-infected cells. If this hypothesis is correct, the results we obtained with formalin-killed syngeneic tumor cells can be explained on the basis of three possible mechanisms: immunological enhancement, immune tolerance or induction of antibody to anti-tumor idiotype. The merits of each mechanism in accounting for the results are discussed.
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PMID:Increased growth of Rous sarcomas in chickens pretreated with formalinized syngeneic tumor cells. 20 68

Resistance to the development of progressively growing tumors induced by Rous sarcoma virus is a dominant trait controlled by a gene linked to the major histocompatibility complex (MHC). The effect of bursectomy (Bx) on the expression of this trait was studied in two inbred lines of chickens homozygous for different MHC alleles, and which differ with respect to the gene controlling resistance to Rous tumors. The results show that Bx alters the expression of the trait, since genetically resistant birds were rendered highly susceptible to progressive tumor growth. The bursa of Fabricius thus makes an important contribution to resistance. The results do not indicate whether genetic resistance is mediated exclusively by B cells or by another bursa-dependent population.
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PMID:Role of B cells in the expression of genetic resistance to growth of Rous sarcoma in the chicken. 20 32

Immunization of CBAT6T6 mice with MC-29 hepatoma antigen did not change the take of Rous sarcoma virus, Schmidt-Ruppin strain [RSV(SR)] mouse tumors after sc transplantation. Immunization with MC-29 hepatoma antigen only slightly increased the average survival time of the mice and significantly decreased tumor growth only at the minimal lethal dose level. Immunization of mice with MC-29 hepatoma antigen and immunization with chicken Rous sarcoma gave similar results; both elicited much less transplantation resistance than immunization with irradiated RSV(SR) mouse tumor cells. The data indicate that there are common tumor-specific transplantation antigens of MC-29 hepatoma and Rouse sarcoma, but further in vitro experiments are needed to prove this.
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PMID:Comparative study of tumor-specific transplantation antigens of MC-29 chicken hepatoma and Rous sarcoma virus-induced sarcomas in mice. 22 8

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

An enzyme treated preparation of saprophytic Mycobacterium phlei, referred as NSI, when administered intramuscularly has been found to protect the chicks against Rous Sarcoma Virus induced tumor. A protection level of 35.4%, 24.1% and 21.2% were observed when challenged on 10th, 20th and 30th day post NSI inoculation. The tumor growth inhibitory-activity of NSI was significant (P less than 0.01). Both, systemic and intralesional administration of NSI exhibited significant tumorostatic activity (P less than 0.05). NSI stimulated the cell mediated immune response to specific as well as to nonspecific Rous sarcoma antigen. These studies indicated the immunopreventive activity of NSI against Rous sarcoma tumor which had an immunogenic basis.
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PMID:Nonspecific immunoprotection against Rous sarcoma tumor in chicks. 255 99

v-src is an effective carcinogen when expressed from Rous sarcoma virus (RSV) in vivo. Whereas RSV tumors require sustained oncogene expression, their growth is largely a balance between viral recruitment of tissues and host immune destruction of infected cells. We have therefore examined the tumorigenic potential of v-src in the absence of viral recruitment and viral antigen expression. v-src was introduced with high efficiency into chicken wing web tissues using replication-defective (rd) retroviral vectors. Clonal sarcomas were induced rapidly, and, furthermore, v-src potentiated metastatic progression in approximately 0.1%-1% of tumor clones with unexpectedly short latency. rd vectors proved effective not only in transducing v-src into tissues but also as insertional markers of tumor clonality. The rd vector present in most primary and metastatic tumors was a highly truncated form of RSV derived by viral transmission of spliced v-src mRNA; this vector should thus avoid viral recruitment and host anti-viral immune reaction through its complete lack of viral structural genes. Under such conditions v-src maintains strong carcinogenicity in vivo when restricted to clonal tumor growth and can confer rapid metastatic potential on a discrete subset of tumor clones.
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PMID:v-src induces clonal sarcomas and rapid metastasis following transduction with a replication-defective retrovirus. 255 19

Rous sarcoma cells were implanted into the kidney of rats. After 5 days of growth the renal tumor was used for comparing histology with glucose 6-phosphatase (G6Pase) enzyme histochemistry (EHC) and 18F-fluoro-2-deoxyglucose (FDG) auroradiography (ARG). It was found that the regions of the kidney tumor that had retained normal kidney structures were devoid of FDG, whereas there was histochemical staining of normal cortical areas. Regions of tumor growth, on the other hand, retained FDG and lacked G6Pase. Necrotic areas did not accumulate FDG. There was a dramatic decrease in the areas of G6Pase activity as a result of tumor infiltration in the kidney. The results show that FDG, currently being evaluated as a tumor detecting radiopharmaceutical indeed accumulates into areas of vital malignant growth, and they indicate that FDG positron emission tomographic (PET) images reveal the true anatomic location of malignant tissue.
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PMID:Tumor localization with 18F-2-fluoro-2-deoxy-D-glucose: comparative autoradiography, glucose 6-phosphatase histochemistry, and histology of renally implanted sarcoma of the rat. 298 66

Six breeding groups of chickens, each characterized by a different haplotype of the B blood group system, were challenged with different classes of antigens, namely Newcastle disease vaccine (ND), infectious bronchitis vaccine (IB), infectious bursal disease viral agent (IBD), Salmonella pullorum antigen (P), and sheep red blood cells (SRBC). Parents were challenged at 20 weeks of age, and their offspring were challenged at 3 weeks of age. Blood samples were taken from the parents at 1 week after challenge, and from the offspring at 1, 2, 3, and 4 weeks after challenge for determination of antibody titers to each antigen. The offspring were also challenged at 8 weeks of age in the wing-web with Rous sarcoma virus (RSV). Tumor scores were taken weekly on individual chickens for the next 10 weeks. There were significant differences (P less than .01) between breeding groups of parents for antibody titer responses to ND, IB, P, and SRBC. There were significant differences (P less than .05) between the breeding groups of offspring for antibody titer responses to ND, IB, IBD, P, and SRBC. There were significant (P less than .01) differences between the breeding groups in the accumulative tumor scores over the 10-week period. The lines that cause regression of Rous sarcomas (R-lines) were significantly (P less than .01) superior in resisting tumor growth to those lines that allow progressive growth of tumors (Pr-lines). The only antigen to which the R-lines gave significantly (P less than .01) higher titers of antibody responses than the Pr-lines was SRBC.
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PMID:Genetic aspects of antibody responses in chickens to different classes of antigens. 370 75


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