Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Fatal polycythemia induced in mice by dysregulated erythropoietin production by hematopoietic cells. 155 41

Animals infected with conventional anaemia (FVA) or polycythemia-inducing (FVP) strains of the Friend virus develop lethal erythroleukaemia. A variant strain, RFV, induces an initially identical disease except that it spontaneously regresses in 50% of infected mice. To determine whether pluripotent stem cells as measured by spleen colony forming units (CFU-s) in leukaemic mice are productively infected with virus and whether their infection influences the outcome of the disease, we tested CFU-s from leukaemic mice for susceptibility to cytotoxicity by monospecific antiviral gp70 antiserum. Spleen CFU-s from progressively leukaemic (FVP, FVA and RFV) mice were productively infected with virus. CFU-s in RFV progressors became infected by 40 days post-virus inoculation. FVA and FVP progressors became infected between 15 and 21 days post virus. Infection of CFU-s was accompanied by an increase in the proportion of replicating (S phase) CFU-s in these populations. Spleen CFU-s from fully regressed RFV regressor mice were uninfected and remained so throughout the course of their disease. Bone marrow CFU-s in both regressors and progressors remained uninfected and were not induced to increased cell cycling.
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PMID:Infection of haematopoietic stem cells in mice with Friend virus induced erythroleukaemia. 346 55

To determine whether hemopoietic cells infected with Friend polycythemia-inducing spleen focus-forming virus (SFFVp) are conserved or suppressed via natural surveillance in leukemia-resistant adult mice, we engrafted C57BL/6 recipients with isologous transgenic (donor origin marker) or natural killer (NK) cell-deficient B6 beige marrow cells exposed to SFFVp in vitro. Both groups of primary recipients were viremic and nonleukemic. Spleen cells from primary SFFVp-infected chimeras were engrafted into irradiated leukemia-susceptible secondary recipients to reveal dormant leukemia and grew as tumors of donor origin in 8 of 38 (21%) and 33 of 47 (70%) instances, respectively. Treatment of marrow donors and recipients with anti-asialo GM1 serum resulted in the depression of NK cell activity and the rapid development of dormant leukemia. We conclude that NK cells are an effective surveillance mechanism able to suppress SFFVp-induced preleukemic stem cells.
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PMID:Natural killer cell suppression of Friend virus-induced preleukemic hemopoietic stem cells. 347 19

We have investigated the effect of 55Fe on the survival in suspension of erythropoietin (epo)-independent erythroid progenitor cells (CFU-E*) induced by Friend polycythemia virus (FV). Spleen cells from C3Hf/Bi mice previously infected with FV were exposed to carrier-free 55Fe, and the survival of CFU-E* as a function of time in liquid medium was determined from the number of erythroid colonies that developed from these cells seeded in plasma cultures without added epo. The results showed that spleen CFU-E* were highly vulnerable to 55Fe: Do approximately equal to 1 h exposure to 100 microCi/ml. Marrow CFU-E* behaved in a similar manner. The 55Fe responsible for their suicide had been presented to the progenitor cells only during the 4-h period of incubation, after which they were washed and plated in excess nonradioactive iron. We therefore conclude that CFU-E* themselves, and not only their progeny, are capable of actively incorporating iron. Under the same conditions in the absence of added epo, the effect of 55Fe on the survival of normal spleen or marrow CFU-E could not be assessed because two few normal CFU-E survived the incubation period. Normal bone marrow cells incubated in complete medium containing epo retained their capacity for erythrocytic colony formation, and CFU-E could then be shown to be vulnerable to 55Fe. Thus, either the iron-incorporating system of normal CFU-E was inducible by epo, or else epo permitted survival of the CFU-E so that the activity of a constitutive iron-incorporating system could be recognized.
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PMID:Erythroid progenitor cells (CFU-E*) from Friend virus-infected mice undergo 55Fe suicide in vitro in the absence of added erythropoietin. 405 46