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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Distribution of 67Ga in different organs of A/H mice bearing a lymphatic leukaemia was examined. Mice received 10(6) leukaemia cells intravenously and groups of 6 mice were sacrificed every other day. Twenty-four hours before sacrifice, the mice received intraperitoneal injection of 67Ga. Spleen, lymph nodes, liver, left kidney, lung, left femur, and a sample of blood were taken, to determine their radioactivity. The maximum of 67Ga uptake was on the 7th day after transplantation of the leukaemia, whereas before death it declined to the values observed in control mice without leukaemia. The changes are interpreted in terms of the ability of leukaemia cells and of macrophages to bind 67Ga.
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PMID:Distribution of 67Ga in organs of mice with lymphoid leukaemia. 123 21

ME26 virus, which was generated by inserting the coding region of the acute avian leukemia-inducing virus E26 into a murine retrovirus vector, encodes a 135-kDa gag-myb-ets fusion protein. Amphotropic murine leukemia virus pseudotypes of ME26 virus induce a high incidence of erythroleukemia 2 to 4 months after injection into newborn NFS/N mice. Spleen cells from the majority of these mice proliferate to high levels in the presence of the erythroid hormone erythropoietin (Epo) and can easily be established as permanent Epo-dependent cell lines. The cell lines contain multiple copies of ME26 viral DNA and express viral message and protein. An Epo receptor mRNA of normal size can be detected in these cells, and binding studies reveal a single class of lower-affinity Epo receptor with an affinity for Epo that is in the range of that previously reported for erythroid cells. The ME26 virus-induced Epo-dependent cell lines, however, appear more immature than previously described erythroid cell lines and more closely resemble early hematopoietic precursor cells, suggesting that the virus may be activating the Epo receptor in hematopoietic cells that do not normally express it. Consistent with this idea, we are able to infect an interleukin-3-dependent myeloid cell line, FDC-P2, with ME26 virus and convert it to Epo dependence. The ME26 virus-infected FDC-P2 cells, even before growth on Epo, showed a large increase in the amount of Epo receptor mRNA. However, no ME26 viral integrations can be detected adjacent to the Epo receptor gene, indicating that the virus is not activating the Epo receptor gene by promoter/enhancer insertion. Our results are more consistent with the hypothesis that the gag-myb-ets-encoded viral fusion protein, which is known to bind DNA, is directly or indirectly activating the expression of the Epo receptor gene in these cells.
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PMID:Induction of erythropoietin responsiveness in murine hematopoietic cells by the gag-myb-ets-containing ME26 virus. 130 43

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

Cyclosporin A (CsA) is an effective modulator of multidrug resistance (MDR) in vitro and in murine tumour systems in vivo. We now report the production of immunity to L1210 leukaemia by the addition of CsA to VP-16 therapy of leukaemic BDF/1 mice. VP-16/cyclosporin A tumour immunity induction arises as a consequence of active therapy independently of immunisation with modified tumour cells. The addition of CsA to VP-16 prolongs survival of BDF/1 host mice bearing L1210 leukaemia beyond that produced by equivalent dose VP-16 alone. A subpopulation of 60-day surviving mice after combined VP-16/CsA are immune to rechallenge with the same leukaemia inoculum to which they were originally exposed. Spleen cells from immune mice adoptively transfer anti-L1210 leukaemia immunity to untreated BDF/1 mice in a dose dependent, statistically significant manner. Adoptive transfer experiments additionally suggest active recruitment of immunologic response in recipient animals: (1) We have been able to perpetuate leukaemia immunity in four sequential cohorts of naive recipient mice. This propogation of adoptive immunity is accomplished by use of spleen cells harvested from each preceeding passively-protected animal cohort; (2) Cyclophosphamide pretreatment of adoptive transfer recipient mice abrogates the ability of their splenocytes to perpetuate passive protection in sequential adoptive transfer experiments.
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PMID:Development of cyclosporin A mediated immunity in L1210 leukaemia. 176 73

Proliferative and interleukin responses to T-cell mitogens such as concanavalin A (Con A) were rapidly and progressively reduced in BALB/c mice infected with the Friend leukemia complex (FLC) or its helper, Friend murine leukemia virus (F-MuLV). In contrast, a combination of the protein kinase C activator phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) and the Ca++ ionophore A23187 elicited a normal lymphoproliferative response up to 8 days postinfection (p.i.) and normal interleukin-2 (IL-2) and interferon-gamma responses up to day 14 p.i. Exogenous IL-2 failed to restore the lymphoproliferative response of infected cells regardless of the stimulation used. These results showed that the T-cell deficits may be at least partly attributable to a derangement of the signal transduction pathway leading to activation. Spleen cells passed through nylon wool columns reacquired a normal responsiveness to Con A +/- TPA up to 14 days p.i. The latter finding suggests that the alterations in signal transduction are not caused by primary defect of the responder-T cells but may result from an extrinsic suppressive mechanism.
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PMID:Alterations of T-cell functions during Friend leukemia complex infection: defective signal transduction? 181 Mar 22

Spleen necrosis virus (SNV) is an avian retrovirus that can infect some mammalian cells such as dog cells as well as all avian cells tested to date. We were interested in testing whether SNV could also infect primate cells. For these experiments, we used HeLa and COS-7 cells. Initially, we determined whether the SNV long terminal repeat promoter was functional in HeLa and COS-7 cells. In transient transfection assays, the SNV promoter efficiently directed chloramphenicol acetyltransferase gene expression in both HeLa and COS-7 cells. Using SNV- and murine leukemia virus-derived retroviral vectors containing the neomycin phosphotransferase gene, we found that SNV established a provirus in HeLa and COS-7 cells as efficiently as did an amphotropic murine leukemia virus, as judged by the number of G418-resistant HeLa and COS-7 cell colonies obtained after infection and selection. Although SNV formed a provirus in both HeLa and COS-7 cells, productive infection of these cells was not obtained with use of replication-competent SNV. These results suggest that SNV can infect, form a provirus, and stably express a transduced gene in primate cells, but there is a posttranscriptional block to its replication in these cells.
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PMID:Spleen necrosis virus, an avian retrovirus, can infect primate cells. 187 Feb 1

A leukemia characterized by the proliferation of undifferentiated hematopoietic stem cells is described from a desert spiny lizard (Sceloporus magister). This is the first neoplasm reported from this species and the first leukemia from the family Iguanidae. A massive invasion of primitive hematopoietic cells was noted in the vascular system and heart muscle. Spleen, bone marrow, lungs, adrenal gland, pancreas, brain, skin, testes, liver, lamina propria and submucosa of intestines were extensively involved. Tissue-fixed mast cells were noted in the kidney and intestinal submucosa but were not participating in the neoplastic proliferation.
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PMID:A case of leukemia in the desert spiny lizard (Sceloporus magister). 192 Jun 80

The spleen was irradiated in 8 patients with chronic lymphatic leukaemia using RTG radiation in doses of 225 to 800 cGy for one treatment course. The follow-up after radiotherapy lasted 12.5 months on average. In 7 cases a considerable reduction was observed in the size of the spleen, and in 6 cases the absolute leucocyte and lymphocyte counts decreased by a mean of 46% and 50% respectively. In patients in late phase of the disease the improvement was short-lasting; 5 patients died (2 from infectious complications). In patients in early phase remissions of 30 months were obtained with normalization of the proportions or T and B cells During the radiotherapy a significant rise was observed in the per cent of granulocytes and a fall of albumin level. Increased gamma-globulin and uric acid levels and decreased hemoglobin level and erythrocyte count were not significant. Variable changes were noted in the platelet count. No bleeding tendency was noted. Spleen irradiation may be used in the treatment of non-Hodgkin lymphoma associated with malignant proliferation prevailing in the spleen, that is in chronic prolymphocytic leukaemia and hairy-cell leukaemia Favourable effects of spleen irradiation were observed in chronic lymphatic leukaemia and this induced us to use this method in our eight cases.
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PMID:[Treatment of low-malignancy lymphomas by spleen irradiation]. 226 Apr 12

The role of Abelson murine leukemia virus (A-MuLV) in the accelerated development of murine plasmacytomas (PCs) (Potter et al., 1973: Science, 132, 592-594) was studied in a new experimental system. Spleen cells from pristane-treated or untreated BALB/c mice carrying Robertsonian 6;15 fusion chromosomes were infected in vitro with helper-free A-MuLV overnight and subsequently transplanted into the peritoneal cavity of pristane-treated or untreated BALB/c mice. Donor-derived PCs developed in 4 out of 76 pristane-treated recipients [latent periods: 38-82 (mean 51) days] that had received spleen cells from pristane-treated donors, and also in 2 out of 41 pristane-treated recipients that had received untreated donor-derived spleen cells (latent periods: 65 and 120 days). Three of the PCs in the former and both PCs in the latter group were tested for integration and expression of the v-abl gene, with positive results. This indicates that the spleen contains PC-precursor cells that can be activated by A-MuLV even before the impact of pristane. All 6 donor-origin PCs carried a translocation involving chromosome 15, band D2/3. Four of these corresponded to a typical 12;15 translocation, one was a variant 6;15 translocation and the 6th may represent a previously unidentified translocation between chromosome 15 and the lambda gene-carrying chromosome 16. No PCs developed among 29 pristane-untreated recipients that had received pristane-treated donor-derived spleen cells. In addition to PCs, monocytic tumors developed in 37 (26%) of all recipients. Their development was independent of pristane treatment of recipients but was particularly frequent in those who had received spleen cells from pristane-treated donors.
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PMID:The accelerating role of Abelson murine leukemia virus in murine plasmacytoma development: in vitro infection of spleen cells generates donor-type tumors after transfer to pristane-treated BALB/c mice. 254 29

The highly metabolized nitrosourea carmustine (BCNU) is an anticancer agent which alkylates DNA and is metabolized to both active and inactive species by cytochrome P-450 enzymes. Other highly metabolized anticancer drugs have altered toxicities when some histamine H2 antagonists are coadministered. To test this hypothesis with BCNU, DBA/2J male mice were given a single injection of cimetidine (CMT 100 mg/kg) or ranitidine (RNT 25 mg) at various times up to 30 min before, or up to 60 min after a BCNU injection. Spleen colony assays for normal bone marrow stem cell viability showed enhanced toxicity for BCNU when CMT was administered concomitantly. In P-388 leukemia-bearing DBA/2J mice, both CMT and RNT significantly enhanced the antitumor effects of BCNU doses of 30 mg/kg. Pharmacokinetic analyses of BCNU elimination in Cd-1 mice showed marked prolongation of BCNU elimination and increased (BCNU concentration) x time products when CMT was concomitantly administered. These results demonstrate that enhanced BCNU bone marrow toxicity and antitumor activity is produced by CMT. The effect appears to be related to impaired drug clearance when the two agents are administered concurrently. RNT slightly enhanced BCNU antileukemic effects, but it did not significantly alter BCNU myelotoxicity nor drug elimination patterns.
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PMID:H2-antagonists and carmustine. 256


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