Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

B.M. cells of RLV-infected BALB/c mice can proliferate in methylcellulose in the absence of E.P., while normal B.M. cells cannot (12). Not only the more primitive BFU-E shows hormone-independency (18). This phenomenon is in favour of the view that the Rauscher virus induced erythroblastosis is a true neoplasia although transplantation experiments failed so far. The experiments in which transformation in vitro of B.M. cells by RLV is established (19) show that the CFU-E can serve as a target for the virus. Treatment of normal mice with CFA leads to a rapid increase in CFU-E in the bone marrow (18). Splenomegaly of RLV-infected mice is enhanced by CFA-treatment probably due to an increase in targets. Transfection with proviral DNA also can transform the CFU-E of BALB-c mice. This approach allows in vitro studies on the resistence of mouse strains to RLV in vitro. The studies are of interest for the human disease in two aspects. In vitro transformation assays are needed to study the oncogenic potential of putative human leukemia viruses. Furthermore the studies have yielded some new insight in the pathogenesis of virally induced erythroblastosis. This might serve as a model for e.g. acute myeloid leukemia in man.
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PMID:Hormone independent in vitro erythroid colony formation by mouse bone marrow cells. 18 23

The purpose of this study was to develop an animal system of protective immunity against oncornaviruses and to test whether such immunization had an inhibitory effect upon chemical sarcomagenesis. Several murine sarcoma virus (MSV) pseudotypes were used as immunogens and tested against themselves, against other pseudotypes, against leukemogenesis by their helper viruses, and against sarcomagenesis by 3-methylcholanthrene. Five MSV pseudotypes were obtained by rescuing complete MSV from MSV-genome carrier, nonproducer hamster tumor cells, using five different leukemia viruses as helpers. The immunogenic properties of these pseudotypes could be specified on the basis of the following observations. 1) They all induced sarcomas in newborn mice and regressing sarcoma nodules in young adult mice. After regression, most mice remained free of neoplastic disease, but some developed sarcoma or leukemia relapses. 2) They had an individual host range pattern, usually determined by the helper virus, as tested by inoculation of a constant virus dose in BALB/c, C57BL/Ka, and Swiss mice. 3) They were all immunogenic, in the sense that the first virus inoculation prevented sarcoma induction by a second challenge, either viral or cellular. 4) They were cross-reactive in vivo, one pseudotype immunizing against another, in the combinations tested. 5) They were able to immunize against leukemogenesis induced by their helper viruses. This was shown by prevention of leukemic deaths by Rauscher and Friend viruses, by a slight prolongation of survival after challenge with the Precerutti-Law leukemia virus, and by inhibition of splenomegaly by Moloney leukemia virus. In a second stage of the study, we investigated whether immunization with any of the MSV psuedotypes had an inhibitory effect upon sarcomagenesis induced by near-threshold doses of 3-methylcholanthrene. The incidence of these sarcomas was essentially the same in virus-immunized and control mice. It was concluded that immunizing procedures able to prevent sarcomagenesis when the inducer is a virus did not have any consistent preventive effect when the inducer was a chemical.
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PMID:Murine sarcoma virus pseudotypes used as immunogens against viral and chemical oncogenesis. 19 61

Experimental evidence for the presence and biosynthesis of subviral, leukemogenic particles in the isolated mitochondria of spleen cells of mice infected with Rauscher murine leukemia (RML) virus is presented. These subviral particles sediment at a density of 1.27-1.29 g/ml and induce splenomegaly and RML three weeks after i.v. or i.p. administration to white mice. Virosomes have been labelled with [32P]phosphate in the isolated mitochondria from RML spleen cells and high molecular weight (70S) [32P]RNA has been isolated from these subviral, leukemogenic particles. Rauscher virus group specific antigens were detected by immunodiffusion in the inner membrane and matrix fraction of the mitochondria of RML spleen cells. These results together with our earlier findings strongly suggest that mitochondria of the transformed cells participate in the biosynthesis of RNA tumor viruses. Possible mechanism of the penetration of viral genetic information of RNA tumor viruses into mitochondria of tumor cells in vivo is discussed.
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PMID:Biosynthesis of subviral oncogenic particles (virosomes) in mitochondria of Rous sarcoma and Rauscher murine leukemia cells. 19 96

One hundred feline leukemia virus-positive cats with evidence of anemia were examined to determine characteristics of the anemia. The anemia was usually normochromic and normocytic, with low reticulocyte counts but with normal white blood cell and platelet counts. About one third of the cats had splenomegaly. The bone marrow was usually hypocellular or normally cellular, with an increased myeloid to erythroid ratio. A history of recent stress or infection in many cases indicated that the immunosuppressive effect of feline leukemia virus may have been involved. Supportive treatment with periodic blood transfusions was successful in prolonging survival. Corticosteroids and androgens may have been beneficial in some cases.
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PMID:Anemia associated with feline leukemia virus infection. 22 95

In general, megakaryocytic myelosis is nowadays considered to be a separate disease entity, one of the myeloproliferative syndromes. Morphologically there are localised or diffuse proliferations of usually large pleomorphic megakaryocytes and immature atypical megakaryocytes up to megakaryoblasts in the bone marrow, in the sense of a haemoblastosis. In the course of the disease megakaryocytic splenomegaly develops. A sarcomatous form (megakaryoblastoma, megakaryo-sarcoma) is rare. Megakaryocytic myelosis may arise from chronic meyloid leukaemia or polycythaemia vera, rarely as a transitional stage to an acute myeloblastic leukaemia or megakaryoblastic leukemia in the sense of a blast crisis. The mature form of the disease, which has an age peak at 59 years and is not sex-linked, often takes a course over years with increasing splenomegaly, anaemia, moderate leucocytosis and usually marked thrombocytosis (average value of 720 X 10(9)/1). Life threatening complications are haemorrhages, thromboembolism and increased frequency of infections due to antibody deficiency in the advanced stage.
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PMID:[Megakaryocytic myelosis: clinical and morphological features (author's transl)]. 26 86

To evaluate the frequency and clinical significance of the Philadelphia chromosome (Ph1) in adult acute leukaemia, bone marrow chromosomes were studied in 15 adults with acute lymphocytic leukaemia (ALL) and 55 with acute nonlymphocytic leukaemia (ANLL). Morphology, clinical findings, therapeutic response and survival were compared in patients with and without the Ph1. The Ph1 was found in six newly diagnosed adults presenting with ALL. Adults with Ph1+ ALL differed from those with Ph1-ALL in being older, in having more frequent lymphadenopathy and splenomegaly and in demonstrating higher initial leucocyte counts and more peripheral blasts. Complete remissions were obtained in all nine adults with Ph1-All but in only three of six with Ph1+ ALL. Adults with Ph1-ALL survived significantly longer. Four adults with ANALL were Ph1+. They did not respond to treatment and survived significantly shorter periods than adults with Ph1-ANLL. No clinical or morphologic features indicated which patients with acute leukaemia would have the Ph1. Since the presence of the Ph1 in acute leukaemia has therapeutic and prognostic significance, marrow chromosome studies should be performed in adults presenting with acute leukaemia, especially ALL.
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PMID:The Philadelphia chromosome (Ph1) in adults presenting with acute leukaemia: a comparison of Ph1+ and Ph1-patients. 26 8

On a prospective fashion during approximately two years, 22 pediatric patients with acute non lymphocytic leukemia were evaluated. Of this population the majority had acute mielocytic leukemia, followed by acute myelomonocytic leukemia. Absolutely all patients at the time of diagnosis and subsequently every 4 to 6 weeks had a bone marrow aspiration test. When the patients were first seen, 54% of them presented fever; lymph node enlargement was not a common finding. Only few of this patients presented splenomegaly and/or hepatomegaly. In regards to complete blood counts the most outstanding of its was the presence of leukocyte count above 20000/mm.3 in 8 of this patients. From the 22 patients studied only 21 are evaluable. All 21 patients were treated with a 4 drug combination (modified COAP). Sixteen patients (76%) achieved bone marrow remission, of which only 15 patients (71%) achieved complete remission. The median duration remission was of 9.2 months with a range of 2 to 26 months. At the present time only 7 patients (33%) are alive and on remission. Two more patients are alive but in full relapse. The mortality rate of this study is of 59%. The review of recent chemotherapy reports is presented and the need for further trials is emphasized especially in view of recent papers published in which it appears that better results are being obtained at last in children's acute non lymphocitic leukemia.
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PMID:[Results of the treatment of nonlymphoblastic acute leukemia in a pediatric population]. 27 Sep 99

The pathophysiology of serially passaged myeloid leukemia of the RFM mouse was studied. The disease was characterized by progressive splenomegaly and infiltration of both marrow and spleen by myeloblasts. The animals became anemic and there was an associated erythroid hyperplasia in the spleen. Leukemic spleen cells obtained from animals early in the course of the leukemia were less malignant than those obtained from preterminal mice. The leukemia is most sensitive to alkylating agents but is also responsive to antimetabolites.
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PMID:Murine myeloid leukemia: I. Pathophysiology and drug sensitivity. 27 Oct 44

Fifty-one adults with acute lymphoblastic leukaemia were entered into a trial of intense initial chemotherapy and early "prophylaxis" of the central nervous system (CNS). Initial treatment with OPAL (Oncovin (vincristine), prednisolone, adriamycin (doxorubicin), and L-asparaginase (colaspase)) followed by craniospinal or cranial irradiation and intrathecal methotrexate produced remission in 36 patients (71%). Seventeen of these patients relapsed three to 18 months after the start of remission; the remainder had been in remission for 12 to 52 months by the end of the study. The predicted median duration of complete remission was 18.5 months. None of the four patients who initially had clinical evidence of CNS disease, three of whom also had leukaemic cells identical to those found in Burkitt's lymphoma, achieved remission. Those patients who initially had hepatomegaly or splenomegaly had a shorter remission than those without. The predicted median survival was 27 months in those who achieved complete remission, one month in those who did not, and 21 months overall. The addition of colaspase and doxorubicin to vincristine and prednisolone and the use of early CNS treatment clearly improved the remission rate among adults with acute lymphoblastic leukaemia, though the presence and length of remission was affected by the extent of disease at presentation. Burkitt-like leukaemia, which had a poor prognosis, is probably a separate disease and may benefit from a different therapeutic approach.
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PMID:Combination chemotherapy for acute lymphoblastic leukaemia in adults. 27 16

Cytopheresis techniques have proven useful in the provision of platelets and granulocytes for transfusion to the pancytopenic patient. Mechanical cell removal has been applied to the treatment of chronic myelocytic and lymphocytic leukemias and the Sezary syndrome. We have treated a 16-year-old pregnant acute myelomonocytic leukemia (AMML) patient for 12 weeks solely with the use of intensive leukopheresis utilizing batch processing centrifugation and packed red cell transfusions. The patient presented with a white blood cell count of 54,000/mm3 with 64% myelomonoblasts, a platelet count of 45,000/mm3, marked gingival hyperplasia, and splenomegaly. Patient had a normal spontaneous delivery of a 2.5-kg male infant without complications. At the time of delivery, 12 weeks later, the white blood count had fallen to 4,9000/mm3 with 8% blasts and the platelet count had risen to over 100,000/mm3. Gingival hyperplasia decreased and the patient felt well. We have treated an additional small group of patients with acute myelogenous leukemia (AML) with high white counts with short term intensive leukopheresis followed by chemotherapy with promising results.
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PMID:Therapeutic leukopheresis of acute myelo-monocytic leukemia in pregnancy. 27 83


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