Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several lines of Friend, Gross, and Rauscher virus-induced rat tumors were able to grow only in Friend, Gross, and Rauscher virus-tolerant rats that had received injections of each of these viruses at birth. When the tumors were transplanted into the virus-tolerant rats that had received injections of the other types of murine leukemia virus (MuLV), they grew initially and then regressed. Tumors did not grow in normal rats. The same is true in the methylcholanthrene-induced tumors that had been infected with MuLVs. It was deduced from these results that the transplantation antigen of tumor cells that were induced by infection with Friend, Gross, and Rauscher viruses may contain an antigen common to all three viruses and also an antigen that is individually specific, and that the host's immunological tolerance (induced by the neonatal injection of either Friend, Gross, or Rauscher virus) may consist of the tolerance common to all three viruses and, also, of the tolerance that is individually specific.
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PMID:Lymphomas and immunological tolerance in the rat induced by murine leukemia viruses. 5 25

New antigenic specificities, not detectable on parental cells and transmissible after the withdrawal of the drug treatment, have been induced in mouse lymphomas. Studies were conducted of proliferative stimulation of syngeneic lymphocytes and the generation of cytotoxic lymphocytes (CL's) in a mixed lymphocyte-tumor cell culture system by 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (DTIC)-induced antigens in L1210 and EL4 leukemia sublines. The DTIC-induced antigens were observed to stimulate [3H]thymidine uptake by normal and primed syngeneic lymphocytes and to generate specific CL's to DTIC-altered cells. The specificity of the in vitro immune reactivity was demonstrated. Characteristics of lymphocyte triggering, including the optimal ratio of stimulating cells to responding cells, the kinetics of CL activation, and the quantitation of CL activity, were also evaluated. DTIC antigens on leukemic cells can activate syngeneic lymphocytes and can act as target antigens in cell-mediated immunity. The experimental data support the transplantation antigen-like nature of DTIC-induced antigens.
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PMID:In vitro lymphocyte stimulation and the generation of cytotoxic lymphocytes with drug-induced antigenic lymphomas. 7 62

A tumor-associated transplantation antigen (TATA) from guinea pig L2C leukemia cells was solubilized by different methods. It was found that the 3 M KCl extraction yielded the most immunogenic TATA of L2C cells. Immunization of normal strain 2 guinea pigs with this extract in complete Freund's adjuvant gave complete protection against a subsequent challenge with tumor cells. Further fractionation of the KCl extract of L2C cells by Sephadex G-200 chromatography suggested that the immunogenic activity was present in the fraction containing materials with estimated m.w. of less than 20,000 daltons.
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PMID:Solubilization and partial characterization of a tumor-associated transplantation antigen of the guinea pig L2C leukemia. 7 74

The possibility that some or all of the viral proteins, gp70, p30, and the histocompatibility antigen, H-2, function as the tumor-specific transplantation antigen (TSTA) of the R-MuLV-induced leukemia, RBL-5, and also in the secondary in vitro induction of cytotoxic T lymphocytes (CTL), was investigated. The antigen was obtained by isolating the plasma membranes of RBL-5 cells and solubilizing with sodium deoxycholate (DOC) followed by gel filtration chromatography. A fraction containing excellent tumor-rejection activity but low amounts of gp70, p30 and H-2 was chromatographed on goat anti-gp 70 goat anti-p 30 and sheep anti-H-2b immunoaffinity columns. The data obtained indicate that gp 70, p 30 or H-2 do not function as TSTA of RBL-5 leukemia, individually or as a complex. Similarly, the antigen responsible for the specific secondary induction of CTL in vitro is distinct from these three proteins.
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PMID:Rauscher leukemia virus-induced tumor antigens: complete separation from gp70, p30 and H-2. 9 83

A review of our current progress in C-type virus vaccine research is presented. This includes the findings of C-type virus or its antigen expressions in every naturally occurring tumor of two strains of "low-incidence" laboratory mice, the BALB/cCr mouse and the NIH Swiss mouse. Vaccine preparation methods are described including the inactivation of C-type virus infectivity with optimal maintenance of the antigen titers of at least two of the polypeptides of the C-type virus, gp69/71 and p30. The cell-mediated immune response of the mouse to C-type virus vaccines, as measured by a footpad assay for delayed-type hypersensitivity and an in vitro lymphocyte transformation assay, is described. Studies with two murine C-type viruses (Rauscher leukemia and Gross leukemia) a simian C-type virus, and an avian C-type virus (avian myeloblastosis virus) showed that the cell-mediated immune response of the animal includes type-specific, group-specific, and interspecies-specific reactivity. The mouse gave a cell-mediated immune response to at least one of the polypeptides of the C-type virus, the gp69/71, whether this polypeptide was presented to the immune system of the mouse as whole virus, Tween-ether-treated virus, or a purified polypeptide. One measure of the effectiveness of the C-type virus vaccines was provided by immunization of the mouse with Rauscher leukemia virus preparation that induced resistance to challenge with both live Rauscher leukemia virus and a naturally occurring BALB/c leukemia virus. Evidence is presented that the C-type virus can act as an effective transplantation antigen in syngeneic tumor cell lines resulting in the immunogenicity and loss of tumorigenicity of these cell lines. An approach to the viral immunoprevention of spontaneously occurring tumors is discussed.
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PMID:An approach to C-type virus immunoprevention of spontaneously occurring tumors in laboratory mice. 17 22

A cultured line of RBL-3 leukemia, induced by Rauscher murine leukemia virus (R-MuLV) in C57BL/6 mice, was found to be a virus nonproducer. An NB tropic virus indistinguishable from R-MuLV, however, was recovered after treatment with 5-iodo-2'-deoxyuridine (optimal concentration, 200 microgram/ml). Dexamethasone treatment slightly boosted the production of the activated virus but did not by itself activate the virus. RBL-3 cells were found to have Fc receptors but no surface immunoglobulin or Thy 1.2 antigen. RBL-3 cells exhibited the Friend-Moloney-Rauscher virus-specific transplantation antigen as shown by its immunosensitivity and immunogenicity in tumor rejection experiments. Crude membrane and crude soluble antigen preparations obtained from RBL-3 cell membranes retained the capacity to induce tumor rejection.
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PMID:Immune reactivity of RBL-3, a nonproducer leukemia induced by Rauscher murine leukemia virus in C57BL/6 mice. 27 20

Cell walls (CW), containing peptidoglycan and carbohydrate, were prepared from Corynebacterium parvum and tested for lymphoreticular stimulation and antitumor effects in CBA-T6T6 mice. CW did not induce splenomegaly. Peritoneal macrophages became cytostatic to Rl leukemia cells in vitro after ip injection of CW or of peptidoglycan but not of carbohydrate; however, on a dry-weight basis the activity was low (less than 10%) compared with that of C. parvum. Tumor outgrowth was significantly suppressed after sc injection of mixture of M4 fibrosarcoma cells and CW, but again the activity of CW was less than 10% of the of C. parvum. In contrast to injection of C. parvum, intratumor injection of CW failed to retard tumor growth in normal mice, although a suppressive effect was found in mice presensitized to C. parvum. Again, unlike C. parvum, CW did not act as an adjuvant for tumor-specific transplantation antigen, as judged by a lack of enhanced resistance to tumor challenge after injection of mixtures of CW and irradiated M4 cells. The distribution and persistence of 125l-labeled C. parvum and CW after sc or ip injection were similar. CW activity was not restored by attachment to oil droplets or emulsification in Freund's incomplete adjuvant.
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PMID:Antitumor activity of purified cell walls from Corynebacterium parvum. 62 69

Five different lines of a strain 2 guinea pig leukemia (L2C) which had been carried in different laboratories share certain chromosomal markers and have a common surface immunoglobulin idiotypic determinant indicating that they have a common origin. All these leukemic lines have on their surface of the B alloantigen (equivalent of the murine H-2K and H-2D antigens) and four of these five lines have on their surface the Ia alloantigens normally present on the strain 2 lymphocytes. The result of a study of the growth and rejection patterns of these leukemias in inbred and random-bred guinea pigs of selected histocompatibility type indicates that both the B and Ia antigens can act as transplantation antigens in guinea pigs. Immunization protection tests in syngeneic animals demonstrated that the four Ia-positive leukemias possessed a tumor-associated transplantation antigen (TATA), while the one Ia-positive leukemias possessed a tumor-associated transplantation antigen (TATA), while the one Ia-negative leukemia by this criteria did not appear to have TATA. However, crisscross immunization protection tests demonstrated that preimmunization of syngeneic animals with an Ia-positive L2C line lead to a subsequent protection against challenge with the Ia-negative leukemia. Immunization with the Ia-negative line never protected against a subsequent challenge with any of the leukemic cells of L2C lines. These results strongly suggest that the Ia-negative leukemia possessed a TATA that can be recognized but is not itself immunogenic, and also indicate that Ia antigens on L2C cells are functionally associated with TATA and can act as immunological carries for tumor transplantation determinants.
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PMID:Mutant lines of guinea pig L2C leukemia. I. Deletion of Ia alloantigens is associated with a loss in immunogenicity of tumor-associated transplantation antigens. 126 83

The specificities of the antisera raised in the CDF1 mice that had been immunized with the P1.HTR tumor cells xenogenized by transfection with recombinant H-2Kb-erbB gene were studied. The antisera cross-reacted with a broad range of tumor cell lines maintained either in vitro or in vivo in an immunofluorescence assay. However, they did not react at all with syngeneic normal tissue cells from thymus, spleen, bone marrow and fetal liver. Even though antigens related to the murine leukemia virus and murine mammary tumor virus (MuMTV) were demonstrated in many of the tumor cell lines tested with specific antibodies, these antigens did not seem to be primarily involved in the anti-P1.HTR antibody activity. The 74 kDa molecule, which was precipitated by the anti-P1.HTR anti-serum from the surface radiolabeled cell extract of P1.HTR tumor and was discriminated from the 70 kDa molecule precipitated by the anti-MuMTV serum, was widely distributed among various tumor cell lines tested, but was absent in normal tissue cells. In contrast to the extensive cross-reaction by the antibody, the cytotoxic T lymphocyte generated in the P1.HTR immune mice were shown to be specific to the P1.HTR tumor, and the 98 kDa molecule was precipitated by the anti-P1.HTR serum from the P1.HTR tumor but not from other tumors tested. It is suggested from these results that the 98 kDa molecule is a candidate for an individual tumor-specific transplantation antigen, and is immunodominant for inducing cytotoxic T lymphocytes to coexisting intrinsic retroviral antigens and other serologically cross-reactive tumor antigens.
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PMID:Characterization of the individual and cross-reactive antigens involved in the anti-tumor immunity induced by use of an H-2K-erbB recombinant gene transfectant. 167 57

DBA/2 (H-2d) mice bearing a transplanted highly metastatic lymphoma (ESb) in a state of widely disseminated disease could be successfully treated by a combination of surgery (removal of the local tumour), irradiation (5 Gy) and adoptive immunotherapy. The immunotherapy was achieved by transfer of anti-ESb-immune spleen cells from B10.D2 mice, which express the same major histocompatibility complex (MHC) molecules as DBA/2. In contrast, anti-ESb-immune cells from MHC-disparate C57BL/6 mice did not confer protective immunity. The B10.D2 anti-ESb-immune T cells contain two types of cytolytic specificity as detected by limiting-dilution analysis: (1) clones with specificity for the ESb-tumour-associated transplantation antigen (TATA) (at low frequency), and (b) clones with specificity for minor DBA/2 histocompatibility (H) antigens (at high frequency). Immune B10.D2 cells raised against different tumour lines or against TATA-ESb tumour variants did not confer the 100% protection seen with immune cells against ESb TATA+ cells. Finally we demonstrate that the allogeneic immune cells are more potent in terms of protective immunity than corresponding syngeneic immune cells. The data suggest that the strong graft-versus-leukemia effect with immune T cells from allogeneic MHC-identical but not from MHC-disparate mice was due to T cells with MHC-restricted specificity for an ESb-associated TATA. A graft-versus-host reactivity that developed much later and could not be prevented was most likely due to T cells sensitized against normal minor H antigens of the host. Our results are of potential relevance for allogeneic bone marrow transplantation and adoptive immunotherapy protocols.
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PMID:Specific eradication of micrometastases by transfer of tumour-immune T cells from major-histocompatibility-complex congenic mice. 182 94


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