Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1261473 (sarcoma)
 25,952 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

Receptors for monkey red blood cells (MRBC) that are expressed on subpopulations of human lymphoid cells are coded by genes linked to the major histocompatibility complex (MHC) region. Since malignant transformation of cells is associated with changes in structures coded by the MHC region, 10 cultured human melanoma and sarcoma cells and autologous SV40-transformed fibroblasts were tested for expression of MRBC receptors and compared with normal autologous fibroblasts. Only 2 of the tumor cell lines and normal fibroblasts from the same individual formed rosettes with MRBC. On the other hand, SV40 transformation induced in all the fibroblasts expression of receptors for MRBC. MRBC receptors on SV40-transformed fibroblasts show properties similar to those on B lymphoid cells.
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PMID:Appearance of receptors for Macaca speciosa red blood cells on human fibroblasts transformed by simian virus 40. 625 61

Inbred SJL/J and A.SW/SnJ mice have been bred to produce (SJL female X A.SW male)F1 and A.SW female X SJL male)F1 mice. F1 mice were then crossed to produce (SJL female X A.SW male)F2 and (A.SW female X SJL male)F2 mice. The inbred, F1, and F2 populations were followed for 2 years to determine the incidences of spontaneous reticulum and sarcoma (RCS) expression. SJL mice had a greater than 90% incidence of RCS, although F1 mice showed almost no RCS. The incidence of RCS in the F2 populations was 24.1%. These data were consistent with the hypothesis that in F1 and F2 populations a single dominant A.SW gene is able to suppress the expression of the pleomorphic RCS disease characteristic of the SJL mouse. This gene was not an H-2 gene, since the two strains were congenic with respect to the major histocompatibility complex; this gene was not on the Y-chromosome, and its phenotypic expression was not inherited in an X-linked manner.
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PMID:Single-gene abrogation of spontaneous pleomorphic SJL/J mouse reticulum cell sarcoma expression. 635 30

The T10 sarcoma, induced in a (C57BL/6J X C3HeB/-FeJ)F1 (H-2b X H-2k) mouse, grows locally (L-T10) and generates spontaneous lung metastases (M-T10). L-T10 cells were found to express the H-2b haplotype, whereas M-T10 expressed both the H-2b and H-2k haplotypes. Most L-T10 cloned cells expressed the H-2b haplotype and were not metastatic. The minority expressed both H-2k and H-2b and were metastatic. Serial transplantations of H-2k-negative clones always ended in spontaneous expression of the H-2k haplotype concomitantly with the acquisition of metastatic potency. The expressed H-2k seemed to be associated with the metastatic properties inasmuch as an H-2b-positive--H-2k-negative clone, which had lost the expressed H-2b and was temporarily H-2 negative, remained nonmetastatic until reexpression of the two haplotypes occurred. Serial transfers of H-2k-positive clones resulted in the maintenance of the expressed H-2k haplotype and the retention of metastatic capacity. A shift toward increased metastatic capacity correlated with H-2k expression occurred during serial transfers of every clone tested. Expression of major histocompatibility complex components, rather than their loss, may potentiate the metastatic capacity of tumor cells.
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PMID:Alterations in major histocompatibility complex phenotypes of mouse cloned T10 sarcoma cells: association with shifts from nonmetastatic to metastatic cells. 657 89

The lysis of murine sarcoma virus-murine leukaemia virus (MSV-MuLV)-induced tumour cells by cytotoxic T lymphocytes (CTL) appears to require that an antigen specified by MSV-MuLV, or induced by the infection, be presented in association with class I major histocompatibility complex antigens. The viral proteins of the tumorigenic MuLV seem to be a part of the antigens recognized by these dually restricted anti-MuLV CTL, but the precise nature of the putative viral antigen(s) recognized by CTL is unknown. Studies using recombinant viruses have suggested that a product of the viral envelope gene (env gene), perhaps the glycoprotein gp70, is the viral antigen recognized by CTL. Attempts to use purified gp70 or anti-gp70 antibodies to block CTL recognition of retrovirus-induced tumour cells, however, have yielded contradictory results. To examine more closely the role of gp70 in the CTL response to MuLV infections, we have constructed murine cell lines which express only the env gene of the Moloney murine leukaemia virus (M-MuLV). We show here that BALB/c-3T3 cells expressing the M-MuLV envelope gene products on their cell surface are susceptible to lysis by M-MuLV-specific CTL.
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PMID:Cytotoxic T lymphocyte recognition of transfected cells expressing a cloned retroviral gene. 660 80

Dendritic cells, the most potent 'professional' antigen-presenting cells, hold promise for improving the immunotherapy of cancer. In three different well-characterized tumour models, naive mice injected with bone marrow-derived dendritic cells prepulsed with tumour-associated peptides previously characterized as being recognized by class I major histocompatibility complex-restricted cytotoxic T lymphocytes, developed a specific T-lymphocyte response and were protected against a subsequent lethal tumour challenge. Moreover, in the C3 sarcoma and the 3LL lung carcinoma murine models, treatment of animals bearing established macroscopic tumours (up to 1 cm2 in size) with tumour peptide-pulsed dendritic cells resulted in sustained tumour regression and tumour-free status in more than 80% of cases. These results support the clinical use of tumour peptide-pulsed dendritic cells as components in developing effective cancer vaccines and therapies.
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PMID:Bone marrow-derived dendritic cells pulsed with synthetic tumour peptides elicit protective and therapeutic antitumour immunity. 748 12

Meth A gp110 has been tentatively identified as a tumor rejection antigen. Following isolation of a class I major histocompatibility complex (MHC)-restricted, CD8+ anti-Meth A cytotoxic T-lymphocyte (CTL), we sought to determine whether the determinant recognized by this CTL was: (a) functional in tumor rejection of Meth A sarcoma; and (b) derived from Meth A gp110. Initially, we isolated an anti-Meth A CTL-resistant variant of Meth A sarcoma, Meth A4R, by immunoselection. The results of the subsequent analysis of Meth A4R cells showed the CTL-defined determinant as having a functional role in transplantation rejection of Meth A sarcoma. Walker et al. (Proc. Natl. Acad. Sci. USA, 89: 7915-7918, 1993) showed that the cationic lipid, N-[1-(2,3-dioleoyloxy)propyl]-N,N,N- trimethylammonium-methyl sulfate, mediated delivery of a recombinant glycoprotein into the cytosol of target cells, making it available for processing and presentation by class I MHC molecules. As a result, the cells were sensitized for cytolysis by a class I MHC-restricted CD8+ CTL, which recognized an epitope expressed by the glycoprotein. In a similar manner, we treated the SV40-transformed BALB/c cell line, SVBalb, which is relatively insensitive to cytolysis by the anti-Meth A CTL, with Meth A gp110 and N-[1-(2,3-dioleoyloxy)propyl]-N,N,N-trimethylammonium methyl sulfate. The sensitivities of the treated cells and control cell lines to the anti-Meth A CTL were then examined. The results of these experiments permit us to conclude that the determinant recognized by the anti-Meth A CTL line is derived from Meth A gp110.
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PMID:Characterization of cloned class I MHC-restricted, CD8+ anti-Meth A cytotoxic T-lymphocytes: recognition of an epitope derived from the Meth A gp110 tumor rejection antigen. 751 21

The finding that class I major histocompatibility complex (MHC)-restricted cytotoxic T lymphocytes (CTL) recognize peptide antigens (epitopes) bound to class I MHC molecules has accelerated efforts to identify CTL-defined tumor peptides for the development of peptide-based cancer immunotherapy. The Meth A sarcoma is probably one of the best studied of all murine tumors. It is extremely lethal unless protective immunity is induced. We recently reported the characterization of a cloned H-2Kd-restricted, CD8+ anti-Meth A CTL line (CTLMA-9C; Frassanito et al., Cancer Res., 54: 4424-4429, 1994). The cytotoxic reactivity of this CTL was shown to be restricted to Meth A sarcoma, and the results of the analysis of the immunogenicity of the CTL-resistant variant of Meth A, designated Meth A4R, indicate that the CTL-defined epitope is functional in tumor rejection. Here we have isolated class I MHC-associated peptides from Meth A sarcoma by mild acid treatment and resolved them into sixty fractions by reverse phase-HPLC. These fractions were then tested for their ability to sensitize the DBA/2 mastocytoma P815 to cytolysis by the anti-Meth A CTL. A single fraction, fraction 27, has been repeatedly identified as containing the CTL-defined epitope. Peptides eluted from the CTL-resistant variant, Meth A4R, failed to sensitize P815 to cytolysis by the anti-Meth A CTL, while fraction 27 derived from Meth A sensitized Meth A4R to lysis by the CTL. These findings confirm the peptide nature of the epitope recognized by CTL on the surface of Meth A. Our future efforts will focus on the identification and sequence analysis of the tumor peptides and the development of a tumor peptide-based vaccine model for immunotherapy.
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PMID:Identification of Meth A sarcoma-derived class I major histocompatibility complex-associated peptides recognized by a specific CD8+ cytotoxic T lymphocyte. 752 38

Traditionally, heat shock proteins (HSPs) are believed to be located intracellularly, where they perform a variety of chaperoning functions. Recently, evidence has accumulated that some tumor cells express HSPs on the cell surface. The present study confirms this finding and correlates HSP72 cell surface expression, induced by nonlethal heat shock, with an increased sensitivity to interleukin-2-stimulated CD3-natural killer (NK) cells. After nonlethal heat shock, a monoclonal antibody directed against the major heat-inducible 72-kD HSP (HSP72) stains the cell surface of sarcoma cells (ie, Ewing's sarcoma cells or osteosarcoma cells) but not that of normal cells (ie, peripheral blood lymphocytes, fibroblasts, phytohemagglutin-stimulated blasts, B-lymphoblastoid cell lines) or of mammary carcinoma cell line MX-1 carcinoma cells. In this study, we show for the first time a correlation of HSP72 cell surface expression with an increased susceptibility to lysis by NK effector cells. This finding is supported by the following points: (1) HLA-disparate effector cells show similar, elevated lysis of HSP72+ heat-treated sarcoma cells; (2) CD(3-) NK cells, but not CD3+ cytotoxic T lymphocytes, are responsible for the recognition of heat-shocked sarcoma cells; (3) by antibody-blocking studies, an immunogenic HSP72 determinant, which is expressed selectively on the cell surface of heat-treated sarcoma cells could be correlated with NK recognition; (4) the reported phenomenon is independent of a heat-induced, transient downregulation of major histocompatibility complex (MHC) class-I expression; and (5) blocking of MHC class-I-restricted recognition, using either MHC class-I-specific monoclonal antibody W6/32 on the target cells or alpha/beta T-cell receptor monoclonal antibody WT31 on effector cells, also has no inhibitory effect on the lysis of HSP72+ tumor cells. Finally, our in vitro data might have further clinical implications with respect to HSP72 as a stress-inducible, sarcoma-specific NK recognition structure.
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PMID:CD3- large granular lymphocytes recognize a heat-inducible immunogenic determinant associated with the 72-kD heat shock protein on human sarcoma cells. 763 45

The inability of the autologous host to reject resident tumor cells is frequently the result of inadequate generation of tumor-specific T cells. Specific activation of T cells occurs after delivery of two signals by the antigen-presenting cell. The first signal is antigen-specific and is the engagement of the T-cell antigen receptor by a specific major histocompatibility complex antigen-peptide complex. For some T cells, the second or costimulatory signal is the interaction of the T-cell CD28 receptor with the B7 activation molecule of the antigen-presenting cell. In the present study, we demonstrate that mouse sarcoma cells genetically engineered to provide both T-cell activation signals stimulate potent tumor-specific CD4+ T cells that cause rejection of both engineered and wild-type neoplastic cells. Two other recent studies have also demonstrated that costimulation via B7 can improve tumor immunity. However, our study differs from these reports by two important observations. (i) One of these studies utilized mouse tumor cells expressing xenogenic viral antigens, and hence, the results are not applicable to wild-type resident tumors. Our study, however, demonstrates that coexpression of B7 by major histocompatibility complex class II+ tumor cells induces immunity in the autologous host that is specific for naturally occurring tumor antigens of poorly immunogenic tumors. (ii) In both earlier studies, only CD8+ T cells were activated after coexpression of B7, whereas in the present report, tumor-specific CD4+ T cells are generated. This report therefore illustrates the role of B7 activation molecule in stimulating potent tumor-specific CD4+ T cells that mediate rejection of wild-type tumors and provides a theoretical basis for immunotherapy of established tumors.
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PMID:Constitutive expression of B7 restores immunogenicity of tumor cells expressing truncated major histocompatibility complex class II molecules. 768 9


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