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)

Intensive antileukemic treatment was evaluated in 22 patients with secondary acute myelogenous leukemia (sAML) and 14 patients with myelodysplastic syndrome (MDS). Results of combination remission-induction chemotherapy were compared with 126 patients contemporarily treated for primary AML. The duration of hypoplasia, induced by remission induction chemotherapy, tended to be longer in the sAML and MDS patients when compared to de novo AML, but reached significance only for the duration of thrombocytopenia: 26 days versus 18 days (P less than 0.01). The number of hypoplastic deaths during remission-induction chemotherapy of patients with sAML and MDS was low. Four of the 36 patients treated for sAML or MDS died during hypoplastic phases induced by remission-induction chemotherapy. The complete remission (CR) rates were similar in primary AML (67%), sAML (62%), and MDS (64%). The CR rates of patients younger than 45 years were 75% for de novo AML, 75% for sAML, and 71% for MDS. Remission rates in patients older than 45 years were identical in the three subgroups but significantly (P less than 0.005) inferior to those obtained in younger patients: 56%, 50%, and 57%, in de novo AML, sAML, and MDS, respectively. The remission duration without bone marrow transplant (BMT) was significantly shorter (P less than 0.01) in MDS and sAML when compared with primary AML. Long-lasting CR in MDS and sAML was only obtained in three of the six patients treated with allogeneic BMT. Intensive antileukemic therapy could be considered in young patients with MDS and life-threatening cytopenias or patients with sAML.
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PMID:Intensive antileukemic treatment of patients younger than 65 years with myelodysplastic syndromes and secondary acute myelogenous leukemia. 238 11

A 12-year old boy was admitted to Saitama Children's Medical Center because of fever and epistaxis. He had leukocytosis (WBC 40,800/microliters, blast 75%), anemia, thrombocytopenia and high levels of serum LDH, lysozyme, Vitamin B12, and plasma histamine. Bone marrow aspiration revealed hypercellular marrow with 31.2% blasts, 15.2% eosinophils, and 14.2% basophils. Blasts had Auer rods and were positive for peroxidase and negative for alpha-naphthyl butyrate esterase and PAS stainings. Ia, CD13 (My7), and CD19 (B4) antigens were expressed on his leukemic cells. Chromosomal study showed 46, XY, t(7;8) (q35;q22), del(9) (q13q22). Southern blot analysis using immunoglobulin constant region (C) probes revealed germline patterns of C mu, C kappa, C lambda, and breakpoint cluster region. A diagnosis of acute myelomonocytic leukemia (AMMoL, M4) was made. He attained a complete remission with daunorubicin and cytarabine, and 6 months later he received bone marrow transplantation from HLA-identical sister. This case had the common breakpoint 8q22 with ANLL with t(8;21) (q22;q22), and was unique AMMoL with proliferation of eosinophils and basophils in bone marrow.
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PMID:[Acute myelomonocytic leukemia (M4) with CD19 antigen expression, eosinophilia and basophilia in bone marrow]. 247 65

The results are estimated of treatment for acute myeloid leukaemia using intensive post-remission therapy with high doses of cytosine arabinoside (HiDAC). Two women and four men aged 18-34 years were treated with HiDAC. None of them had been given maintenance or boost chemotherapy any more at the time. The patients were rated for the duration of granulocytopenia and thrombocytopenia for the incidence of non-haematological complications and for the duration and quality of survival. The preliminary results are promising and in keeping with those reported by similar clinical centres abroad, namely that maintenance therapy should be phased out in the presence of intensive post-remission treatment.
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PMID:[Intensive post-remission therapy of acute myeloid leukemia with high doses of cytosine arabinoside]. 258 68

Intensive antileukemia treatment was evaluated in 22 patients with untreated secondary acute myelogenous leukemia (sAML) and 14 patients with bad prognosis myelodysplastic syndrome (MDS). Results of combination remission-induction chemotherapy were compared with 126 patients treated for primary AML. The duration of hypoplasia tended to be longer in the sAML and MDS patients when compared to de novo AML, but reached significance only for the duration of thrombocytopenia: 26 days versus 18 days (p less than 0.01). The complete remission (CR) rates were similar in primary AML: 67%, sAML: 62%, and MDS: 64%. The CR rates of patients younger than 45 years were 75% for de novo AML, 75% for sAML, and 71% for MDS. The number of hypoplastic deaths during remission-induction chemotherapy of patients with sAML and MDS was low. Four of the 36 patients treated for sAML or MDS died during subsequent hypoplastic phases induced by remission-induction chemotherapy. The remission duration without bone marrow transplantation (BMT) was significantly shorter (p less than 0.03) in MDS and sAML, when compared with primary AML. Longlasting complete remissions in MDS and sAML were only obtained in 3 of the 6 patients treated with allogeneic BMT. Intensive antileukemic therapy should be considered in young patients with MDS and life-threatening cytopenias or patients with sAML or RAEBt.
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PMID:Intensive chemotherapy for patients with myelodysplastic syndromes and acute myelogenous leukaemia younger than 65 years. 269 96

The authors examined 117 consecutive patients with acute leukemia within a few days of diagnosis. Sixty-six patients had acute nonlymphocytic leukemia, and 51 had acute lymphocytic leukemia. Forty-two percent of the patients had abnormal ocular findings related to leukemia. The authors found an association between the presence of intraretinal hemorrhages and thrombocytopenia for all patients. In addition, patients with acute lymphocytic leukemia and intraretinal hemorrhages had lower hematocrit levels than did those without such hemorrhage. The presence of anemia was related to the findings of white-centered hemorrhages in patients with acute nonlymphocytic leukemia. The presence of cotton-wool spots was not associated with hematologic parameters. Intraretinal hemorrhages, white-centered hemorrhages, and cotton-wool spots were all found more frequently in adults than in children.
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PMID:Leukemic retinopathy. Relationship between fundus lesions and hematologic parameters at diagnosis. 274 81

A case of AML accompanied by HTLV-I associated myelopathy (HAM) is reported. A 37-year-old woman was admitted to our hospital in April 1985 because of severe anemia, general malaise and fever. On admission, anemia, thrombocytopenia and leukocytosis consisting of 32% myeloblasts and 6% promyelocytes were noted. A bone marrow study revealed marked myeloid hyperplasia, and a diagnosis of acute myelogenous leukemia (M2) was made. In order to improve the patient's severe anemia and thrombocytopenia, a large amount of blood transfusion was applied at once. Thereafter BHAC-DMP therapy was commenced resulting in complete remission 3 months after initiating chemotherapy. Hematological improvement has continued (as of May 1988). In June 1986 the patient showed a gait disturbance of slowly progressive course. Neurological examination revealed hyperactive knee and ankle jerks with a positive Babinski's sign, and foot clonus were also noted bilaterally. Sphincter impairment was detected. A CSF sample contained slight pleocytosis with some abnormal lymphocytes similar to those found in adult T cell leukemia. Antibodies to HTLV-I were found in the CSF and serum by EIA method. According to these findings we diagnosed the patient's illness as HAM, referring to the new clinical entity named by Osame. This patient had undergone a blood transfusion 14 months before the onset of this myelopathy, therefore the transmission of exogenous antigens through blood transfusion may be the cause of HAM. Corticosteroid pulse treatment was administered and striking improvements countering gait disturbance resulted in this patient.
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PMID:[Acute myelogenous leukemia accompanied by HTLV-I associated myelopathy (HAM) caused by blood transfusion]. 274 79

In an effort to increase the proportion of patients with acute myeloid leukemia (AML) remaining in continued complete remission (CCR), we administered intensive postremission consolidation therapy with high-dose cytarabine (Ara-C) and daunorubicin. Eighty-seven patients, with a median age of 38 years (range, 7 to 71), received consolidation therapy after first complete remission was obtained with standard induction chemotherapy that included conventional doses of Ara-C. Consolidation therapy consisted of from one to three cycles of high-dose Ara-C (3 g/m2 intravenously [IV] over 1 hour every 12 hours for 12 doses) followed by daunorubicin (30 mg/m2/d IV bolus for 3 days). After completion of the high-dose Ara-C and daunorubicin, no further therapy was administered. Myelosuppression encountered with consolidation resulted in a median duration of neutropenia and thrombocytopenia of 3 weeks. Four patients (5%) died during consolidation due to infection and/or hemorrhage; 59% of patients experienced severe but nonfatal infectious or extramedullary organ toxicity. With a median follow-up of more than 3.5 years from diagnosis, the proportion of patients, by Kaplan-Meier product-limit estimate, remaining in CCR is 49% (95% confidence limits, 37% to 61%). In a Cox multivariate analysis, only age significantly (P less than .001) influenced the probability of remaining in CCR. The probability of remaining in CCR was 83%, 50%, and 23% for age groups of 25 or less, 26 to 45, and more than 45 years, respectively. These survival curves all have stable long-term plateaus, suggesting cure. In this study, the administration of brief, intensive nonmarrow ablative chemotherapy resulted in a large proportion of patients with AML remaining in CCR, results similar to those reported with allogeneic bone marrow transplantation. Relapse of acute leukemia was still the major reason for therapy failure, suggesting that more effective or additional postremission therapy will be required to further improve the likelihood of cure especially for older patients.
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PMID:High-dose cytarabine and daunorubicin as consolidation therapy for acute myeloid leukemia in first remission: long-term follow-up and results. 236 Sep 32

A 55-year-old woman developed a secondary leukemia following 1-year treatment of Hodgkin's disease. She was admitted to our hospital because of the celiac lymphadenopathy. Open laparotomy was performed. Biopsy specimens of the lymph node demonstrated Reed Sternberg cells with mature lymphocytes. She was diagnosed as having Hodgkin's disease (lymphocyte predominant type). She was treated by the combination chemotherapy consisting of mitoxantrone, cyclophosphamide, vincristine and prednisolone for Hodgkin's disease in November 1986. Hodgkin's disease achieved complete remission and she was regularly followed. No abnormal findings were observed in the peripheral blood and bone marrow. But thrombocytopenia and the blastoid cells appeared in the peripheral blood in February 1988. The bone marrow specimen was hypercellular and occupied by 90% of blastoid cells that were positive for peroxidase staining. She was diagnosed as having AML from the bone marrow aspiration and biopsy specimens. She did not respond to several chemotherapy regimens and now she is treated by low dose Ara C.
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PMID:[Acute myeloid leukemia after the treatment of Hodgkin's disease]. 276 76

From a group of 276 elderly patients studied in the last 12 years in a department of nuclear medicine for investigating a chronic thrombocytopenia, 36 patients have an acquired disorder, with normal platelet life span, a normal megakaryocytic bone marrow count, and absence of any evident cause at the time of clinical evaluation. During the 2 to 10 subsequent years, 16 patients developed symptoms of the myelodysplastic syndrome, i.e., chronic aregenerative anemia, granulocytopenia, dysmyelopoiesis, and appearance of circulating blast cells; three of them died from acute myeloblastic leukemia. So a pure thrombocytopenia due to a platelet production defect, without any demonstrated functional platelet defect or morphologic dysmegakaryocytosis, may be a preleukemic syndrome. In the other 20 patients, with the same pure chronic thrombocytopenia, no malignant evolution has been seen with long follow-up delays, which is often also the case in pure refractory anemias. In the absence of objective criteria of a possible premalignant disorder, the classification of these cases is difficult, which it is also the case for the so-called refractory anemias. We suggest to individualize, in the classification of the myelodysplastic syndromes, a group of pure refractory thrombocytopenias. From a practical point of view such a diagnosis may be useful, at least to avoid inefficient and possibly harmful treatments.
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PMID:Chronic pure thrombocytopenia in elderly patients. An aspect of the myelodysplastic syndrome. 281 58

pSV2 neomycin DNA was electroporated into exponentially growing WEHI-3B D+ cells, and clones containing integrated pSV2 neomycin DNA were selected by treatment with the antibiotic Geneticin. Southern analysis after Eco RI or Bam HI and Hind III digestion demonstrated that two clones, Y1 and Y2, stably incorporated a single copy of intact pSV2 neomycin DNA into different sites. Exposure of parental WEHI-3B D+ cells to retinoic acid, aclacinomycin A, or adriamycin resulted in their differentiation to mature granulocytic cells. Clone Y1 had growth kinetics and numbers of differentiated cells comparable to those of the parental line when exposed to these differentiation-inducing agents. Furthermore, this clone was leukemogenic in BALB/c mice. The disease presented as a moderate anemia, a peripheral blood granulocytosis, a shift in the differential to immature granulocytic forms, and a thrombocytopenia. Although there was no change in bone marrow cellularity, in situ hybridization to identify the presence of the neomycin resistance gene mRNA indicated infiltration of leukemia cells (up to 30%) into this tissue compartment. The observed hematological parameters were indicative of a late stage of disease resembling human acute nonlymphocytic leukemia. Clone Y1, therefore, would appear to be an in vivo model of acute nonlymphocytic leukemia that may be useful for the development of therapeutic strategies to more successfully treat these diseases. Because we have demonstrated that this line is capable of differentiation in vitro and can be stably carried in vivo, it would also be useful for the identification of therapeutic agents capable of initiating the differentiation of leukemia cells in situ.
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PMID:Development of neomycin-resistant WEHI-3B D+ murine cells as an in vivo model of acute nonlymphocytic leukemia. 291 37


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