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Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 56 year old patient with acute myelogenous leukemia (FAB classification: M2), in whom the number of mature myeloid cells similar to those seen in Ph-negative chronic myelogenous leukemia increased markedly 2 months after the diagnosis of refractory anemia with excess of blasts (RAEB). This is a rare case of leukemic evolution as a terminal event of RAEB.
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PMID:Transformation of refractory anemia with excess of blasts into acute myelogenous leukemia with Ph-negative chronic myelogenous leukemia-like characteristics. 229 65

A 44-year-old previously healthy male was diagnosed as anemic and treated at a nearby hospital. A year later, he was admitted to our hospital for precise examination of the progression of refractory anemia. Blood examination showed hemolytic anemia and more detailed examination of this hemolysis revealed pyruvate kinase deficiency. The activity was 15.1% of a normal control. Pyruvate kinase activities of his family members were normal or slightly decreased. Ten months after admission to our hospital, 2% of blast cells with Auer's body in the peripheral blood were noted which increased progressively. The bone marrow contained 17.3% of blast cells with a subsequent diagnosis of acute myelogenous leukemia being made. Although intensive chemotherapy was performed, the patient achieved a brief remission and died 2 years after admission to our hospital.
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PMID:Patient with pyruvate kinase deficiency developed acute myelogenous leukemia. 232 7

We report on eight patients who were 35 to 77 years old with an isochromosome 17q as the sole structural chromosomal anomaly. Additional numerical chromosomal changes were a trisomy 8 or 17 in two cases each and a trisomy 19 in one case. Five patients had myelodysplastic syndrome (MDS) diagnosed according to the FAB nomenclature as chronic myelomonocytic leukemia (CMML) in two cases, refractory anemia with excess of blasts in transformation (RAEBt) in two cases, and refractory anemia with excess of blasts (RAEB) in one case. One patient suffered from a myeloproliferative disorder (MPS). All cases progressed to acute nonlymphocytic leukemia (ANLL) type M1, M2, or M4 in a period of 2 to 30 months after initial diagnosis, except one patient with RAEBt who died within 2 months. Two patients presented with ANLL-M2 at time of diagnosis. Treatment during the chronic phase of disease consisted of mild cytoreduction and/or substitution of platelets or red blood cells. One patient with CMML received an allogeneic bone marrow graft and relapsed after 33 months with ANLL-M1. Treatment results for overt leukemia were poor, and survival was short, lasting from 1 to 4 months. Overall survival was 1 to 37 months (median duration, 6.5 months). Molecular studies in two cases revealed neither a BCR rearrangement nor a translocation of the ABL protooncogene, as observed in Ph1-positive chronic myeloid leukemia (CML). Thus, an i(17q) anomaly seems to identify a distinct subgroup of mostly myelodysplastic and, less frequently, myeloproliferative disorders that progress rapidly to ANLL, respond poorly to chemotherapy, and are associated with short survival after transformation.
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PMID:Isochromosome 17q in Ph1-negative leukemia: a clinical, cytogenetic, and molecular study. 222 38

Hematological and cytogenetic characteristics of 75 cases of therapy-related acute non lymphoid leukemia (t-ANLL) occurring in Hodgkin's disease (HD) are analysed in this multi-institution study. Combined radio and chemotherapy had been given in 88 per cent of patients, either as adjuvant (44 per cent) or as salvage modality (44 per cent). Radiotherapy alone and chemotherapy alone had been given in 3 per cent and 9 per cent respectively. Eighty per cent of patients were in remission of HD and 71 per cent off-therapy while developing leukemia. The median latent time from remission of HD to leukemia was 34 months. The myeloblastic variety of leukemia accounted for 43 per cent of total cases; the myelomonocytic and monocytic for 17 per cent and 4 per cent, the promyelocytic and erythroblastic variants for 5 per cent and 7 per cent of t-ANLL. Twenty four per cent of cases were unclassifiable; one of these was TdT-positive. Dysplastic features of erythrocytic line were invariably present with circulating erythroblasts; defects of granulocytes, circulating megathrombocytes and micromegakaryocytes were also present. Bone marrow hypoplasia and marked fibrosis were documented in 47 per cent and 30 per cent of cases. Preleukemia heralded overt leukemia in 73 per cent of cases; 37 per cent had refractory anemia with no excess of blasts; 16 per cent of preleukemias were unclassifiable. Cytogenetics revealed chromosome abnormalities in 83 per cent of cases; 72 per cent presented chromosome 5 and/or 7 monosomy or partial deletion (5q- or 7q-) of the long arm (94 per cent in the combined modality therapy group). In 3 cases, a pure monosomy 7 was observed; in none 5q-alone. Response rate to conventional therapy was 14 per cent; low and high-dose cytarabine were of little benefit. Long-term CR (28 + and 16 + months) was achieved in 2 cases with allogeneic bone marrow transplantation (BMT) as first-line therapy. A better knowledge of t-ANLL in HD and new therapies, including BMT, may improve the prognosis of this late complication of intensive HD treatment.
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PMID:Treatment-related leukemia in Hodgkin's disease: a multi-institution study on 75 cases. 243 31

We studied chromosomes of BM cells from four neurofibromatosis (NF) patients with leukemia. One patient had a normal diploid karyotype in the chronic phase of juvenile chronic myelogenous leukemia (JCML). When the the leukemia evolved into the accelerated phase, she had cells with 46,XX,-7,+der(7)t(3;7)(q21;p22); the abnormalities resulted in a partial 7p deletion. In another patient with JCML, BM cells in the accelerated phase had 45,XY,-7. The abnormal cells with monosomy 7 disappeared from the BM after chemotherapy but reappeared later in the course. Another patient developed refractory anemia with excess of blasts in transformation (RAEB-T) and had cells with 46,XX,-6,+r(6)(p23?q21?); the abnormalities resulted in partial 6p and 6q deletions. The other patient with ANLL had cells with 45,XX,-7. Our findings and review of data on nine other patients suggest that BM cells of NF patients with JCML in chronic phase have no microscopically detectable chromosome changes and that cells with chromosomal deletion emerge when JCML evolve into the accelerated or blast phase. Thus, deletion of the whole or part of certain chromosomes, such as chromosomes 6, 7, etc., may be an important step towards the evolution of JCML cells or the development of de novo acute leukemias in NF patients.
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PMID:Chromosome pattern in juvenile chronic myelogenous leukemia, myelodysplastic syndrome, and acute leukemia associated with neurofibromatosis. 249 96

A 67 year-old man was admitted to our hospital because of cough and sputum. He smoke one pack of cigarettes a day for more than twenty years and the chest X-ray film revealed a mass in the left hilum and left sided pleural effusion. The diagnosis of small carcinoma of the lung (limited disease, T4N1MO, stage 3B) was made by trans-bronchial lung biopsy and radiographic studies. Both chemotherapy (nimustine (ACNU), cyclophosphamide, vincristine, and methotrexate) and radiation therapy was started, however, the chemotherapy was discontinued in July 1987 because of severe anemia. The diagnosis of refractory anemia with excess of blasts in transformation (RAEB in T) was made by bone marrow aspiration and the patient was treated by transfusion (400-800 ml/week). In December 1987 transition to acute myeloblastic leukemia was confirmed by another bone marrow aspiration biopsy and the patient was given low dose cytosine arabinoside (Ara-C). The response was favorable in the beginning but in about two months pancytopenia became refractory and the patient died in June 1988. Clinically there was no sign of local or distal recurrences of lung cancer, and the complete remission of small cell lung cancer (SCLC) was confirmed by autopsy. Survival in SCLC remains poor, so that the choice of treatment is still the primary concern, however, development of other malignancies which include acute leukemia is another problem which should be taken into account when the treatment is extensive.
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PMID:[Acute myeloblastic leukemia development in a patient with small cell lung cancer in complete remission]. 256 Sep 98

The cytogenetic follow-up of a case of refractory anemia with excess of blasts (RAEB) that rapidly evolved to acute myeloblastic leukemia (M1-FAB type) is described. Bone marrow analysis at presentation revealed two chromosomally abnormal clones that shared an interstitial deletion of the long arm of chromosome 5 (5q-) and a terminal deletion of the short arm of chromosome 12 (12p-), but that differed from one another in the localization of a very similar segment of chromosome 17 (i.e. 17q11-12qter) on two clearly distinct karyotypic sites: 2q37 and 17q25. Fourteen percent of the metaphases examined bore the 2q+ marker and 38% the 17q+ marker; the remaining cells had a normal karyotype. A second study carried out 4 months later, at onset of the acute phase, revealed that the clone with normal karyotype had almost completely disappeared and that there had been an inversion in the ratio of the two abnormal cell populations. In the final study, made 1 month before death, the cells with t(2;17) had totally effaced the other clone. These findings seem to indicate that, among the karyotypic changes that occurred in an original clone with 5q- and 12p-, only the t(2;17) could have played a crucial role in the final leukemic transformation.
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PMID:Evolution of multiple cytogenetic clones and leukemic transformation in a case of myelodysplastic syndrome. 261 26

A patient with M2-ANLL and a 46,XX,del(5)(q22q33), t(2;11)(p21;q24) karyotype is described. The diagnosis was made after a short period of myelodysplastic syndrome. After chemotherapy consisting of Daunorubicin and Arabinosylcytosine in continuous infusion, the patient reached a complete remission. The chromosome pattern described here has been observed in two other patients with refractory anemia and refractory anemia with excess of blasts, respectively. The breakpoints on the chromosomes 2, 5 and 11 allow us to hypothesize the involvement of N-myc, c-fms, GM-CSF and IL-3 genes.
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PMID:5q- and t(2;11) in a patient with M2 acute non-lymphocytic leukemia. Case report. 262 43

Certain hematopoietic disorders and immunodeficiency states are known to carry a risk of developing acute nonlymphocytic leukemia. In the past some of them have been classified by a variety of terms ranging from refractory anemia to preleukemia, but are currently grouped into a new concept of the myelodysplastic syndromes (MDS). The purpose of this article is to briefly review the updated knowledge of the MDS with emphasis on the clonal origin, natural history and mechanisms of leukemogenesis.
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PMID:[Preleukemic disorders]. 264 30

Low-density blood cells from patients with refractory anemia with excess of blasts (RAEB) and RAEB in transformation (RAEB-T) release a high molecular weight inhibitory substance that reduces the entry of normal progenitor cells of granulocytes and macrophages (CFU-GM) into the S-phase. Out of 20 patients with refractory anemia (RA and RAS) only 3 were positive. One patient with CMML was negative. Serial examination of 3 patients (two RA and one CMML) revealed that the production of the inhibitory activity preceded the development of the disease into RAEB, RAEB-T, or AML. With one exception, the inhibitory activity in positive cases was neutralized by antiserum against human placental ferritin.
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PMID:Inhibitor of normal granulopoiesis produced by cells of MDS patients. 270 26


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