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)

Thymus-derived leukemia virus of AKR/J mice was inactivated by anti-theta antiserum. But it was not inactiviated by the antiserum which had been absorbed with intact thymus cells of AKR/J or RF/J mice, and by anti-uterus-derived leukemia virus antiserum. In contrast, uterus-derived leukemia virus of the strain was not inactivated by anti-theta antiserum, but was neutralized by anti-uterus-derived leukemia virus antiserum. The results suggest the possibility that some constitutents of the envelope of thymus-derived leukemia virus are derived from the plasma membrane of thymus cells of AKR mice at the time of budding and that such constituents are not associated with the enveloped of uterus-derived leukemia virus.
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PMID:A positive difference in nature of envelopes of thymus- and uterus-derived leukemia viruses of AKR mice. 6 71

Leukaemia cells of 11 children with acute lymphatic leukaemias (ALL) and lymphoma cells of 4 children with lymphosarcoma (LS) were studied for the presence of T- and B-lymphocyte markers on their cell membranes. Spontaneous rosette formation (E-rosettes) of the malignant cells after adding sheep erythrocytes and the reaction with antithymocyteserum in cytotoxic test served as T-cell-markers and the surface immunoglobulins as B-cell-markers. The leukaemia cells of 5 ALL-patients with mediastinal tumours formed E-rosettes and reacted with the anti-thymocyte-serum. Six ALL-patients did not show these reactions. None of the ALL-patients had surface-immunoglobulins. Two of the 4 LS-children were E-rosette-positive, the cells of the other two LS-children contained surface immunoglobulins. There was a good correlation between the formation of E-rosettes and the reaction with the anti-thymocyte-serum. After absorption of the anti-thymocyte-serum with peripheral leukocytes it reacted with some of the E-positive lymphoblasts and thymocytes but not with normal peripheral T-lymphocytes. Anti-leukaemia-sera against the ALL-cells with T-cell markers of two patients after absorption with spleen cells did not react with peripheral lymphocytes but did effect lysis of thymocytes. Consequently, leukaemia cells which are E-rosette-positive possess a T-lymphocyte-associated antigen and a Thymus-associated antigen.
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PMID:[Serological diagnosis of the antigenic markers of acute lymphatic leukaemias and non-Hodgkin lymphomas in childhood (author's transl)]. 30 96

Thymus-leukemia (TL) antigens are expressed in murine lymphocytes under strict developmental regulation. To elucidate the molecular basis of TL expression, we have identified the molecular species that react with TL antiserum. At least three species can be resolved by metabolic radiolabeling of thymocytes and ASL1 leukemia cells, lysis, immune precipitation, and sodium dodecyl sulfate-polyacrylamide. After a brief incubation with [35S]methionine, the only radioactive molecule recognized by TL antiserum is a homogeneous species with an apparent Mr of 45,000 daltons. This molecule, 45K TL, includes high-mannose-type carbohydrate attached to a 45,000 dalton glycosidase-resistant backbone. In this form, 45K, it is never exposed on the cell surface. If pulse-labeled cells are further incubated with nonradioactive methionine before lysis, however, radioactivity disappears from the 45K TL species and appears in the slower migrating species 46K and 48K TL. Thus, 46K and 48K appear to represent products generated from the 45K TL precursor by posttranslational modification. These TL forms are displayed on the cell surface; they lack high-mannose carbohydrate but evidently include acidic complex-type carbohydrate. Normal thymocytes from Qa:Tla-negative mice lack not only the surface forms of TL but also the intracellular 45K TL form. Peripheral lymphoid cells of Qa:Tla-positive mice synthesize none of these TL species. But the TL antiserum, which contains Qa antibody, recognizes a distinct gene product in spleen and thymus of Qa-Tla-positive mice. In its pulse-labeled form, this molecule, which may represent Qa-1, has an apparent Mr of 44,000 daltons, and consists of a glycosidase-resistant polypeptide core of only 35,000 daltons linked to more high mannose carbohydrate than 45K TL.
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PMID:Synthesis and processing of molecules bearing thymus leukemia antigen. 31 85

Infection of adult C57BL/6 mice with variants of the radiation leukemia virus resulted in variable leukemia incidence. One variant, designated D-RadLV, induced lymphatic leukemia in 0 to 25% of mice after virus inoculation directly into the thymus of young adult mice. The leukemia incidence could be increased to 80 to 100% by host exposure to x-rays. The second variant, A-RadLV, induced lymphatic leukemia in 80 to 100% of similarly inoculated mice without the need for additional radiation treatment. Adult mice were inoculated with D-radLV or A-RadLV. Both variants reduced the immune response to sheep erythrocytes whereas only D-RadLV had an immunosuppressive effect after immunization with a thymus-independent immunogen polyvinyl-pyrrolidone (PVP). Results of transfer experiments indicated that the immunosuppressive effects were expressed at the immunocompetent cell level. Thymus-derived cells were affected by A-RadLV since their immunocompetent function was impaired, whereas D-RadLV affected the marrow cell population of immunocytes. Exposure of D-RadLV-inoculated mice to x-rays induced functional impairment of both thymus and marrow cells. Since the radiation leukemia virus induces "T" lymphatic leukemia it could be proposed that the initial tropism of the virus to thymocytes would lead to high leukemia induction potential, whereas virus tropism to bone marrow cells would yield a low leukemia incidence. The coleukemogenic effect of x-rays could perhaps be related with its capacity to alter and introduce a change in virus-lymphoid cells interaction.
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PMID:Immunologic characteristics in relation to high and low leukemogenic activity of radiation leukemia virus variants. I. Cellular analysis of immunosuppression. 32 Feb 61

Treatment of adult AKR mice with tissue-specific mitotic inhibitor mol. wt. 1,000--20,000 extracted from the AKR thymus significantly delayed the onset of spontaneous thymus leukaemia, whereas extracts of other organs were without effect. A slight prolongation of survival time was found with spleen extract when administered to BALB/c mice infected with Rauscher virus, which causes leukaemia starting in the spleen. Thymus extracts of MW 100,000--300,000 caused myocardial degeneration in some leukaemic and nonleukaemic mice.
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PMID:Effect of tissue specific mitotic inhibitors on survival time of spontaneous and virus-induced murine leukaemia and influence on myocardial degeneration. 69 24

The presence of H-2-linked gene products on spermatozoa and their time of appearance during spermatogenesis was determined. Thymus leukaemia antigen specificities 1, 2 and 3 could not be detected on spermatozoa by absorption of the antisera. Immunofluorescent studies with anti-Slp sera did not reveal any specific reactivity with target spermatozoa. In contrast, H-2D antigens were present on somatic as well as germ line components in testes so the time of their first appearance during spermatogenesis could not be precisely specified. Cell separation experiments indicate that H-2D antigens are present on pachytene spermatocytes and increased in quantity on spermatids. The sperm-specific isoenzyme of phosphoglycerate kinase, Pgk-2, appears at a later stage of spermatogenesis than do the H-2 region antigens.
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PMID:Gene expression of a region of chromosome 17 during murine spermatogenesis. 92 52

Primary lymphoid tumor cells induced by wild type or recombinant Moloney murine leukemia viruses were inoculated intravenously into sublethally irradiated, syngeneic mice and compared for their ability to reestablish in the recipient thymus and spleen. Lymphoid tumors induced by one recombinant, M-MuLV(myc), containing the v-myc oncogene from the avian MC29 retrovirus consistently reestablished in the thymus and spleen of recipient mice. Since tumors in the recipient thymus and spleen could have arisen by infection of host cells, or could reflect an expansion of a minor subpopulation from the donor tumor, we verified the donor and clonal origin of these tumors by Southern blot analysis using a virus-specific probe. As few as 500 of these tumor cells could migrate to the thymus via the blood and flourish in that microenvironment. In contrast, the majority of tumors induced by wild type M-MuLV or two other M-MuLV recombinants not containing v-myc sequences, inefficiently reestablished in the thymus of recipient mice following i.v. inoculation, although splenic tumors developed. These tumors could, however, multiply within the recipient thymus when inoculated intrathymically. Thus, the inability of tumors induced by wild type M-MuLV or M-MuLV recombinants lacking v-myc to reestablish in the thymus following i.v. inoculation appears to reflect inefficient 'thymic homing' rather than the ability to grow in the thymic microenvironment. Collectively, our data suggest that the thymic homing ability of M-MuLV(myc)-induced tumor cells is related to the presence of v-myc sequences or to the cell type transformed by M-MuLV(myc). Thus, we suggest that these cells may provide a useful model for studying how blood-borne metastatic cells, and possibly normal lymphocytes, enter the thymus by way of the microvasculature.
Thymus 1992 Aug
PMID:Induction of thymus-reestablishing lymphoid tumors by a murine leukemia virus carrying the avian v-myc oncogene. 132 92

Retrovirus infection, cocaine administration, and nutritional deficiencies are known to individually produce impairment of the immune system. Therefore, we developed a murine model to study the effect of daily cocaine administration, protein malnutrition, and retrovirus infection causing murine AIDS on the lymphoid cell populations of the thymus. C57BL/6 female mice fed a diet containing 4% protein were studied following chronic cocaine administration and LP-BM5 murine leukemia virus (MuLV) infection. Cocaine administration reduced body and thymus weight. Cocaine partially prevented thymus enlargement due to lymphoid cell proliferation induced by murine retrovirus infection. Cocaine treatment affected dramatically the thymus of protein-malnourished mice where the absolute number of Thy 1.2+, CD4+ and CD8+ cells represented only 10% of the control values. Daily saline injection also induced a significant decrease in the number of Thy 1.2+, CD4+ and CD8+ cells per thymus. These results suggest that the thymus glands of mice fed a low protein diet were susceptible to stress. Retrovirus infection provoked a decrease in the percentage and absolute number of Thy 1.2+, CD4+ and CD8+ cells in the thymus. This effect was potentiated by cocaine treatment. Therefore, cocaine was able to potentiate the impairment of the immune system caused by MuLV infection. We consider that cocaine could alter the immune system by altering the expression of T cell differentiation markers after direct interaction with thymocytes or through the neuroendocrine-thymus axis. Moreover, this effect was more dramatic and severe during protein malnutrition.
Thymus 1992 Nov
PMID:Alteration of thymic cell subsets by cocaine administration and murine retrovirus infection in protein undernourished mice. 133 87

Thymus humoral factor-gamma 2 (THF gamma 2), an octapeptide important for T-lymphocyte regulation, was assessed for its effect on the in vitro growth of human hematopoietic progenitor cells. This was achieved using a recombinant granulocyte-macrophage colony-stimulating factor (rGM-CSF)-stimulated myeloid cell colony formation (granulocyte-macrophage colony-forming cells, GM-CFC) assay as well as a recombinant erythropoietin (rEpo)-stimulated erythroid burst formation (erythroid burst-forming units, BFU-E) assay. Cells were obtained from bone marrow (BM) and peripheral blood (PB) of normal healthy donors and from patients with suppressed bone marrows. The latter group included aplastic anemia, leukemia, and lymphoma patients and patients with solid tumors who responded to intensive chemotherapy with significant pancytopenia. THF gamma 2 significantly enhanced normal BM and PB GM-CFC and PB BFU-E by 2- to 2.5-fold. This effect was totally dependent on the presence of the respective growth factors, that is, rGM-CSF or rEpo, and was specifically reversed by an anti-THF gamma 2 antiserum. Furthermore, although THF gamma 2-induced enhancement of GM-CFC colony formation was not affected by lymphocyte or monocyte depletion, the augmenting effect of the peptide on BFU-E was completely abrogated in the absence of lymphocytes. THF gamma 2-induced augmented growth of progenitor cells derived from severely suppressed marrows was minimal. However, cells from moderately neutropenic patients with leukemia in remission or with lymphoma under chemotherapy responded to the peptide similarly to cells from normal donors. These results suggest a stimulatory role for THF gamma 2 on human myeloid and erythroid hematopoietic progenitor cells. They also suggest the lymphocyte dependence of BFU-E enhancement and lymphocyte independence of GM-CFC stimulation by THF gamma 2. In the former case the thymus-derived peptide may act through the induction of certain erythroid-enhancing lymphokines.
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PMID:Thymic humoral factor-gamma 2, an immunoregulatory peptide, enhances human hematopoietic progenitor cell growth. 154 85

Mice with intraperitoneally inoculated leukemia L1210 cells had a lower total number of thymocytes and a markedly reduced percentage of L3T4+ Lyt2+ (CD4+ 8+) thymocytes, but increased subpopulations of L3T4+ Lyt2-, L3T4- Lyt2+, L3T4-Lyt2-. The percentage of Thy 1.2+ thymocytes was unchanged as compared with control animals. A similar effect was observed is suggested that leukemia L1210 cells produce some activities which diffuse through 0.22 microns filters and influence the subpopulations of thymocytes.
Thymus 1991 Nov
PMID:Changes of thymocyte subpopulations induced by activities diffusing from leukemia L1210 cells. 178 32


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