Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 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 spleens of rats were studied by light and electron microscopy during the course of an acute myelogenous leukemia, with special reference to infiltration of leukemic myeloblasts in the spleens and to the correlation of leukemic cell infiltration with splenic hematopoiesis and splenomegaly. Leukemic myeloblasts infiltrated the cordal space of the red pulp. Many of them appeared in groups. Even in spleens which were heavily infiltrated, leukemic myeloblasts did not penetrate the while pulp. Massive infiltration and proliferation of the leukemic myeloblasts in the red pulp resulted in splenomegaly. The spleen increased its hematopoietic activity, while the medullary hematopoiesis diminished due to the invasion of leukemic myeloblasts in the bone marrow. Compensatory splenic hematopoiesis occurred in most of the leukemic spleens, but diminished in spleens which were very heavily infiltrated with leukemic myeloblasts. Thus, the degree of splenomegaly and splenic hematopoiesis did not necessarily correspond to the percentage of leukemic myeloblasts in the bone marrow, but rather related to the number of leukemic myeloblasts present in the spleen. A possible role for the splenic sinus walls in promoting compensatory hematopoiesis in the spleen is discussed. A consistent association of type "C" virus particles with leukemic myeloblasts was observed.
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PMID:An electron microscopic study of the spleen of the rat in an acute myelogenous leukemia. 26 72

Because no conclusive evidence as to the efficacy of maintenance chemotherapy in acute myelogenous leukemia (AML) existed, a study to obtain such information was done. Twenty-six adult patients with AML in whom complete remission had been achieved following induction chemotherapy were randomly assigned to receive either maintenance chemotherapy consisting of cytarabine and 6-thioguanine for two days each month or to receive no maintenance therapy. The data showed a significant difference in remission duration between the two groups, with median remission lengths for the maintained and unmaintained groups being 10.3 and 6.7 months, respectively (p<.05). In 46 percent of the maintained patients there were remissions lasting longer than 11 months, whereas in none of the unmaintained patients was there such a prolonged remission. No significant drug-induced toxicity was observed. That the prolonged exposure to these chemotherapeutic agents, which were also used in our induction program, did not adversely affect the rate of successful reinduction therapy was shown by identical 50 percent complete remission rates for second inductions in both groups. In patients with palpable splenomegaly at the time of diagnosis, there was no prolongation of remission with maintenance therapy. These data indicate the potential utility of maintenance chemotherapy for prolonging remission duration in acute myelogenous leukemia.
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PMID:Remission maintenance therapy in acute myelogenous leukemia. 26 13

A total of 78 patients with acute leukemia [69 acute lymphoblastic leukemia (ALL) and 9 acute myeloblastic leukemia (AML)] survived more than 4 years. In the years between 1958 and 1967 the number of patients with ALL in Argentina who survived 4 years was 1%. This increased to 21% in the years between 1967 and 1972. The major cause of this increase was the initiation in 1967 of protocols of therapy on a national scale through a cooperative group known as GATLA. In AML patients the number of long-term survivals remained unchanged during both periods. A large percent of the long-term survivors had lower WBC, a higher platelet count, and no hepato- or splenomegaly, lymphadenopathy, or hemorrhagic manifestations at diagnosis. However, only for those patients with a WBC under 100,000/mm3 at diagnosis was there a significant prognostic implication (p less than 0.01). Patients with acute lymphoblastic leukemia who survive more than 4 years without relapse have about an 80% chance of long survival. For those who have lived 4 years with one or more lapses, there is only a 17% chance of long survival, and of these only those who develop extramedullar relapse (CNS or testicular) without bone marrow involvement have a chance of long survival. Patients who live 4 years in continuous complete remission have the same chance of very long survival regardless of previous therapy.
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PMID:Long-term survival in acute leukemia in Argentina: a study of 78 cases. 26 4

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

Two children who presented initially with a lymphoid malignancy were noted to develop recurrences with myeloid features late in the course of their disease. In both cases, evidence of lymphoid differentiation was present in the myelogenous cells that were Ph1 chromosome negative. The first patient had acute myelogenous leukemia and developed a recurrence with morphologic features of acute myelogenous leukemia. Terminal transferase was present in the myelogenous blasts. The second patient initially had a diffuse lymphoblastic non-Hodgkin lymphoma. During the course of her illness she developed a myeloproliferative disorder characterized by basophilic meningitis, splenomegaly, and hypereosinophilia. Lymphocyte T-cell (E-rosette) markers were present on the eosinophils. These observations lend further support to the hypothesis of varying lymphoid and myeloid differentiation in certain cases of leukemia.
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PMID:Myelogenous leukemia evolving during the course of lymphoid malignancy in children. 29 24

This study is based upon an analysis of the hematologic and pathologic material from seven patients with acute myelosclerosis, as well as a review of the literature of 49 cases reported under this designation, or one of its synonyms. Patients with this disease characteristically present with pancytopenia, minimal or absent anisocytosis and poikilocytosis, and a fibrotic bone marrow showing hyperplasia and immaturity of all three cell lines, with particular prominence of megakaryocytes and their precursors. In addition, clinical splenomegaly is almost always absent, and the disease has a rapidly fatal course. We consider only one-fourth of the cases reported in the literature to have the clinical and hematologic features consistent with the diagnosis of acute myelosclerosis; the remainder represent a variety of myeloproliferative disorders, including chronic myelosclerosis with an accelerated terminal phase, acute myeloblastic leukemia with bone marrow fibrosis, myeloproliferative diseases that cannot be subclassified, and cases in which the data are insufficient for analysis. Using strict clinical and hematological criteria, acute myelosclerosis can be separated from other myeloproliferative disorders as a distinct clinicopathologic entity.
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PMID:Acute ("malignant") myelosclerosis. 36 69

This report describes three cases of an atypical variant of agnogenic myeloid metaplasia characterized by pancytopenia, high peripheral blast cell count, lack of significant splenomegaly or tear-drop poikilocytosis, and diffuse marrow fibrosis with an abnormal proliferation of megakaryocytes. It is suggested that these cases represent an acute variant of agnogenic myeloid metaplasia that is distinct from either the terminal blastic transformation of myelofibrosis or acute granulocytic leukemia.
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PMID:Acute myelofibrosis: a report of three cases. 85 Oct 94

Nine patients were selected according to the following criteria: 1. Hematological findings consistent with the diagnosis of myelofibrosis with myeloid metaplasia (MMM), except for an excess of blasts in the blood and bone marrow; 2. No previous (silent) phase of MMM. 3. No PH1 chromosome, and 4. No identifiable cause of secondary myelofibrosis. These patients had either an acute or subacute myelofibrosis. The onset of such symptoms as fever, bone pain, hemorrhage and mild splenomegaly was rapid. Terminal acute leukemia or more often progressive bone marrow biopsy showing myelofibrosis with persistence of differentiated myeloid tissue, particularly megacaryocytes. Isotopic studies (59Fe and 51Cr) showed splenic erythroid metaplasia, poor bone marrow 59Fe uptake and increased peripheral red blood cell destruction. This study confirms that malignant myelosclerosis is a well-defined syndrome which must be distinguished from: a) Acute transformation of typical agnogenic myeloid metaplasia even though it was previously undiagnosed (4 cases of MMM illustrating this possibility have been reported); b) Acute myeloblastic leukemia with myelofibrosis; and c) Myelofibrosis secondary to lymphomatous or carcinomatous bone-marrow invasion (2 cases with acute myelofibrosis appearing long after appropriate treatment have been reported).
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PMID:[Acute or subacute myelofibrosis]. 95 Nov 81

Foam cells in the spleen, bone marrow, liver and lymph nodes were examined on the 73 reliably recorded and sampled leukemia autopsy cases encountered at Kobe University from 1958 to 1972. Although the substances stored in the foam cells were biochemically unknown, the foam cells in leukemia could be morphologically classified into two types: The one was identified with the Gaucher type, but the other was not identified with the sea-blue type and might be considered as to be the transitional type described in another report. Foam cells could be found in the spleen of 6 out of 12 cases of chronic myeloid leukemia, one out of 2 cases of chronic lymphatic leukemia, one out of 7 cases of leukemic lymphosarcoma, one out of 9 cases of acute lymphatic leukemia, and none in 3 cases of monocytic leukemia. In acute myeloid leukemia, the incidence of foam cells in the spleen was 47.5% in 40 cases, and acquired lipidoses were more frequently seen in cases under 19 years of age, in male cases, in cases with an enlarged spleen over 400 g, and in cases of over 4 months' duration.
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PMID:Secondary lipidosis in leukemia. 99 40


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