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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The proliferative activity of bone marrow from Rauscher Leukemia Virus infected mice was studied during the course of the disease. Spleen colony assay and thin-layer agar technique, both presumably reflecting the number of pluripotent hemopoietic stem cells, showed a 2.6 times increase in colony forming units (CFU-S resp. CFU-A) at 12 days after infection. The Bradley method of culturing colonies in agar, which is stated to reflect the number of myeloid precursor cells, resulted in a slower rise in colony forming units (CFU-C) with a maximum of 2.3 times increase at 19 days after infection. These results were compared to the differentiation patterns of the bone marrow at similar intervals after infection. The course of the CFU-C curve parallelled the rise in the number of the myeloblasts in the bone marrow. The pattern of CFU-A and CFU-S curves preceded the rise in number of CFU-C by 7 days. It was found, that RLV infection apart from causing an erythroblastosis in the spleen and a severe anemia is followed by a disappearance of neutrophil granulocytes from the bone marrow. The latter phenomenon is probably the primary cause of the increase of hemopoietic stem cells.
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PMID:The relation between the proliferative activity and the differentiation pattern of bone marrow cells from Rauscher leukemia virus infected BALB/c mice. 122 10

C57BL/6J murine bone marrow cells, infected with a retroviral vector (MP Zen) carrying a monkey erythropoietin cDNA, were transplanted into lethally irradiated syngeneic recipients to study the effect of erythropoietin production by hemopoietic cells. High levels of erythropoietin were recorded in the plasma (median value: 1.2 u/ml) and in media conditioned by peritoneal, spleen, and bone marrow cells from recipient mice. In transplanted mice, the hematocrit was elevated (90 +/- 5%) and the mice died at a mean of 71 days after transplantation. In the blood, platelet counts were usually low and nucleated blood cells slightly elevated. Spleen weight increased 5-fold and bone marrow cellularity decreased slightly. There was a 9.9-fold increase in erythroblast numbers, a 2-fold reduction of lymphocytes, and no variation of the myeloid cells when the total cellularity of bone marrow, spleen, peripheral blood, and peritoneal cells were considered. Calculation of the total numbers of progenitor cells in these organs revealed a 18-fold increase in erythroid colony-forming units (CFU-E) but no significant variation of the erythroid burst-forming units (BFU-E), and myeloid progenitor cell numbers. A variable proportion of CFU-E, (12% or 24% in bone marrow or spleen, respectively) was able to proliferate in unstimulated cultures. Erythropoietic amplification occurred in the spleen and there was a redistribution of the BFU-E and myeloid cells from the bone marrow to the spleen. No significant extramedullary erythropoiesis was seen. This study emphasizes the erythroid specificity of erythropoietin and shows that elevated dysregulated erythropoietin production by hemopoietic cells leads to a fatal polycythemia without erythroid neoplastic transformation.
Leukemia 1992 Feb
PMID:Fatal polycythemia induced in mice by dysregulated erythropoietin production by hematopoietic cells. 155 41

The hematopoietic disregulation in adult mice induced by the malignant histiocytosis sarcoma virus (MHSV) and the Harvey murine sarcoma virus (Ha-MuSV), which both possess c-Ha-ras-related oncogenic sequences, was investigated. Spleen focus formation induced by MHSV and Ha-MuSV was not restricted by the Fv-2 resistance locus in congenic DDD and C57BL/6 mice, unlike leukemogenesis induced by Friend virus, Rauscher virus, and the myeloproliferative sarcoma virus (MPSV). C57BL/6 mice were much more resistant to MHSV and Ha-MuSV-induced spleen focus formation than DDD mice regardless of their Fv-2 state. Infection of DDD mice with MHSV caused a systemic histiocytic neoplasia, best described as murine malignant histiocytosis. Transformed histiocytic cells proliferated excessively in the bone marrow, spleen, and lymph nodes and, in the final stages of the disease, in all major parenchymal organs. The Ha-MuSV caused a strikingly different benign histiocytic tumor in DDD mice and, unlike MHSV, did not induce a rapid, progressive splenomegaly in C57BL/6 mice. Infection of DDD mice with MHSV induced a rapid and synchronized depletion of early and late erythroid precursor cell pools. In MHSV-infected C57BL/6 mice comparable changes were observed with dissimilar kinetics. Macrophage colony-forming cells of MHSV-infected mice were increased in number and proliferated independently of stimulating growth factors. The disease induced by MHSV in mice can thus serve as a model for malignant histiocytosis in humans.
Leukemia 1987 Jan
PMID:Murine retrovirus-induced malignant histiocytosis, an experimental model for the disease in humans. 282 12

Spleen cells from BALB/c or CAF(1) mice released little or no detectable leukemia virus when cultured 2-7 days in vitro. In contrast, spleen cells of CAF(1) mice previously inoculated with parental BALB/c spleen cells released leukemia viruses in 10 of 11 cases studied. Cultures of a mixture of spleen cells from normal BALB/c and CAF(1) mice also contained leukemia viruses. Phytohemagglutinin induced the transformation of lymphocytes in cultures of CAF(1) or BALB/c spleen cells, but this transformation did not activate leukemia viruses. It is concluded that mixed lymphocyte cultures in vitro, just as graft-versus-host reactions in vivo, can activate leukemia viruses that are normally present in a repressed form. This activation is not solely a function of lymphocyte transformation. The activated mouse leukemia virus may subsequently account for the observed high incidence of neoplasia in graft-versus-host disease.
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PMID:Activation of leukemia viruses by graft-versus-host and mixed lymphocyte reactions in vitro. 440 35

To specify the mechanism whereby inoculation of sarcoma viruses protects against leukemia development by leukoviruses, several experiments were performed using Friend virus complex (FVC) and MSV-F, a sarcoma virus pseudotype prepared in vitro with FVC as source of the helper component. The sarcomatous lesions induced by MSV-F were self-limited, irrespective of dose and route of inoculation and protected against the progressive, lethal erythroleukemia induced fy FVC. The sera of MSV-F primed mice had high FVC-neutralizing titers, Out of 3 properties titered in FVC, immunogenicity, XC-syncytium-forming activity and lethality, the frmer two were retained at high titers in MSV-F, while lethality was almost entirely lost: the dose-range between lethal immunizing dilutions was 2-3 logs broader for MSV-F than for FVC. It is postulated that the lethal, early erythroleukemia inducing component (Spleen Focus Forrming Virus) is rapidly lost from FVC upon in vitro propagation. The rescued MSV-F would carry a hightitered, immunogenic and Xc-syncytium forming component (Lymphatic Leukemia Virus), thus behaving as an immunogenic virus of limited pathogenicity.
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PMID:Immunity to Friend virus complex: analysis of protection with a sarcoma virus pseudotype. 625 97

Spleen cells collected from DBA/2 (H-2d) mice inoculated with the polycythemic variant of Friend-Leukemia Virus Complex (FLV-P) were tested for T-dependent immune functions, such as the in vitro generation of cytotoxic T lymphocytes (CTL) and of non-specific T suppressor lymphocytes (STL). CTL were generated against H-2b splenocytes, and STL were obtained following a 5-day lymphocyte culture without stimulator cells. A progressive and severe impairment of the generation of both CLT and STL was found from 2 weeks onward after infection, being almost totally abolished 3-4 weeks after virus challenge. Suppressor cells (SC) capable of inhibiting CTL generation was detected in FLV-P bearing mice. Suppressor activity was unaffected by anti-Thy 1.2 serum and complement but was removed following iron-magnet depletion or passage through nylon-wool column. Moreover complete recovery of the competence of CTL generation was attained when FLV-P infected splenocytes were passed through nylon-wool column. It is concluded that FLV-P infection depresses T-dependent cytotoxic and suppressor responses in mice, by the appearance of non-T adherent phagocytic cells, capable of impairing CTL generation in vitro.
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PMID:Impairment of in vitro generation of cytotoxic or T suppressor lymphocytes by Friend leukemia virus infection in mice. 645 95

Resistance and/or susceptibility for Friend leukemia virus (FLV)-induced leukemogenesis was examined in the fully H-2 incompatible C57BL/6 (B6)-->C3H radiation bone marrow chimeras (RBMC). The results indicated that B6-->C3H chimeras never developed FLV-induced leukemias when infected with FLV 4 months after bone marrow transplantation (BMT). Spleen cells from B6-->C3H chimeras that were preimmunized with 100 Gy-irradiated FBL-3 cells (FLV-induced leukemic cell line originated from B6 mice) were shown to generate anti-FBL-3 specific T-cell proliferation as well as cytotoxic T cells. We also found that when bone marrow cells from B6 mice were mixed with those from C3H mice and then grafted into supralethally irradiated C3H mice, resulting chimeras whose peripheral blood contained less than 30% C3H-derived (susceptible) cells were refractory to FLV-induced leukemogenesis. On the other hand, when C3H mice were infected with FLV and then supralethally irradiated 5 days later and grafted with bone marrow from B6 donors, they developed leukemias which were of B6 origin. Athymic nu/nu mice of B6 background were again shown to develop leukemia following infection with FLV. Possible implication of these findings on the role of T cell-mediated immune response in resistance to FLV-induced leukemogenesis and the immunocompetent nature of fully H-2 incompatible RBMC were discussed.
Leukemia 1993 Jul
PMID:Friend leukemia virus-induced leukemogenesis in fully H-2 incompatible C57BL/6-->C3H radiation bone marrow chimeras. 832 Oct 19

Malignant lymphomas often have complex, nonrandom chromosomal abnormalities. Hepatosplenic gammadelta T cell lymphoma (gammadelta TCL) is an unusual post-thymic T cell lymphoma that primarily involves liver and spleen, often in young adult males. Few cases have had cytogenetic analysis. We report a consistent isochromosome 7q [i(7q)] abnormality in three cases of hepatosplenic gammadelta TCL, one with i(7q) as the sole abnormality at presentation. Three patients, 15-, 37- and 65-year-old males, presented with hepatosplenomegaly and fevers. Histopathologic, immunophenotypic, and molecular genetic studies supported the diagnosis. Spleen, liver, and bone marrow contained sinusoidal infiltrates of atypical lymphoid cells of T cell immunophenotype. PCR performed on two cases demonstrated clonal T cell receptor gamma gene rearrangements. Cytogenetic analysis of bone marrow showed i(7q) as the sole abnormality at presentation in one case. The second case showed i(7q) in addition to two normal chromosomes 7, and other structural and numerical abnormalities. The third case showed i(7q) and a deletion in the long arm of chromosome 11. These findings support the proposal that i(7q) represents the primary nonrandom cytogenetic abnormality in hepatosplenic gammadelta TCL, and plays a role in its pathogenesis.
Leukemia 1997 Aug
PMID:Isochromosome 7q: the primary cytogenetic abnormality in hepatosplenic gammadelta T cell lymphoma. 926 94

Humic substances are formed during the decomposition of organic matter in humus, and are found in many natural environments in which organic materials and microorganisms are present. Oral administration of humus extract to mice successfully induced effective protection against experimental challenge by the two subspecies, Trypanosoma brucei brucei and T. brucei gambiense. Mortality was most reduced among mice who received a 3% humus extract for 21 days in drinking water ad libitum. Spleen cells from humus-administered mice exhibited significant non-specific cytotoxic activity against L1210 mouse leukemia target cells. Also, spleen cells produced significantly higher amounts of Interferon-gamma when stimulated in vitro with Concanavalin A than cells from normal controls. These results clearly show that administration to mice of humus extract induced effective resistance against Trypanosoma infection. Enhancement of the innate immune system may be involved in host defense against trypanosomiasis.
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PMID:Protective effect of humus extract against Trypanosoma brucei infection in mice. 1905 36

Spleen size ranks among the most important risk factors in chronic myeloid leukemia (CML), but the pathogenic mechanisms of splenic hematopoiesis in CML remain poorly defined. Here, we studied the biology of Bcr-Abl positive leukemia-initiating cells in the spleen, using an inducible transgenic mouse model of CML. Disease kinetics showed greater increases of immature leukemic cells in spleen vs bone marrow (BM). To assess how Bcr-Abl alters the behavior of spleen-derived CML cells, we transplanted these cells either before ('pre-uninduced') or 44 days after ('pre-induced') expression of the oncogene. Mice transplanted with pre-induced spleen cells showed significantly increased neutrophilia and splenomegaly compared with mice receiving pre-uninduced spleen cells, suggesting that Bcr-Abl expression in the donors had increased splenic tumor burden. However, pre-induction also altered the biology of these cells, as shown by a striking increase in erythropoietic potential. These results differ from those of BM-derived CML stem cells where pre-induction of Bcr-Abl had previously been shown to decrease disease transplantability. Moreover, splenic cells were less sensitive to imatinib than BM cells. In conclusion, Bcr-Abl alters the biology of splenic leukemic stem cells by a cell-autonomous mechanism, but the disease phenotype is also influenced by the microenvironment of these cells.
Leukemia 2012 May
PMID:Leukemic spleen cells are more potent than bone marrow-derived cells in a transgenic mouse model of CML. 2219 68


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