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)

Data obtained on 88 patients with refractory anemia or preleukemia, without previous cytotoxic treatment, showed medullar chromosomal abnormalities in 32%. In 45% of the cases, the disease had progressed to acute nonlymphocytic leukemia. A high frequency of acute transformation (78%) was observed in patients with abnormal clones. These results are different from those of the Second International Workshop on chromosomes in Leukemia. The discrepancies may be related to the difference between the cases selected for submission to the workshop and those of this study. Serial studies on 28 patients with abnormal karyotypes showed that two different populations of patients were investigated: one with a terminal smoldering phase of leukemia and the other with true preleukemic disease. In the latter group, no predictive karyotype evolution was seen.
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PMID:Cytogenetic study of 88 cases of refractory anemia. 682 68

Two female patients, 42 and 30 years old, respectively, died of acute nonlymphocytic leukemia 43 and 38 months, respectively, after a subsequent treatment: chemotherapy for one and irradiation and chemotherapy for the other, following excision of a malignant glioma. At the time of death, both seemed to be in complete remission of their brain tumor. Both had been treated with procarbazine and nitrosoureas. The latter were responsible for severe myelosuppressive episodes and seem to have played an essential role in the induction of the leukemia. In one case, a myelodysplasia was observed before the onset of the AL and the diagnosis of refractory anemia with excess of blasts seemed warranted. Secondary acute leukemias are rare in the evolution of malignant gliomas and the usefulness of subsequent radiochemotherapy cannot be questioned at the present time. The risks involved in this therapy are minor when compared to the short-term fatal prognosis of this type of tumor.
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PMID:Two cases of acute leukemia following treatment of malignant glioma. 686 Oct 68

Twenty patients are described who received chemotherapy for the diagnosis of acute myeloid leukemia but who were subsequently reclassified as having dysmyelopoietic syndrome using the French-American-British criteria. Thirteen patients had refractory anemia with excess blast cells (RAEB) (age range, 23-82 years; median, 68) and seven had chronic myelomonocytic leukemia (CMML) (age range, 44-79 years; median, 70). Three patients (two with RAEB and one with chronic myelomonocytic leukemia) had previously been treated with cytotoxic therapy for another malignancy. In 15 patients the antileukemic therapy was a chemotherapy regimen that was highly active in acute nonlymphoblastic leukemia (ie, containing daunorubicin and/or cytarabine). These patients achieved complete remission lasting 14, 34+, and 36+ months and survival times of 31, 35+, and 37+ months. All three patients were from a subgroup of four patients characterized by RAEB, younger age, no previous cytotoxic therapy, and treatment with an aggressive chemotherapy regimen. The median survival time of the patients not achieving remission was 1 month (range, less than 1-22). Our results suggest that while most patients with the dysmyelopoietic syndrome appear to have their life shortened by chemotherapy, there is a subgroup characterized by younger age, absence of previous cytotoxic therapy, and the morphologic picture of RAEB who can have a favorable response to aggressive treatment.
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PMID:Effect of chemotherapy for the dysmyelopoietic syndrome. 694 53

The clinical and laboratory features of 37 patients with variants of acute monocytic leukemia are described. Three of these 37 patients who had extensive extramedullary leukemic tissue infiltration are examples of true histiocytic "lymphomas." Three additional patients with undifferentiated leukemias, one patient with refractory anemia with excess of blasts, one patient with chronic myelomonocytic leukemia, one patient with B-lymphocyte diffuse "histiocytic" lymphoma and one patient with "null" cell, terminal deoxynucleotidyl transferase-positive lymphoblastic lymphoma had bone marrow cells with monocytic features. Another patient had dual populations of lymphoid and monocytoid leukemic cells. The true monocytic leukemias, acute monocytic leukemia (AMOL) and acute myelomonocytic leukemia (AMMOL), are closely related to acute myelocytic leukemia (AML) morphologically and by their response to chemotherapy. like AML, the leukemic cells from the AMMOL and AMOL patients form leukemic clusters in semisolid media. Cytochemical staining of leukemic cells for nonspecific esterases, presence of Fc receptor on the cell surface, phagocytic ability, low TdT activity, presence of surface "ruffles" and "ridges" on scanning EM, elevations of serum lysozyme, and clinical manifestations of leukemic tissue infiltration are features which accompanied monocytic differentiation in these cases.
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PMID:The acute monocytic leukemias: multidisciplinary studies in 45 patients. 700 98

The case of a 74-year-old woman with macrocytic, refractory anemia, typical changes in the bone marrow and a 5q-chromosome in bone marrow cells is presented and the literature of this newly described hematological disorder is reviewed. The syndrome is characterized by partial deletion of the long arms of a chromosome No. 5 in bone marrow cells. The chromosomal anomaly is acquired and originates most probably from a pluripotent hematologic stem cell. Hematologic changes are (1) macrocytic, refractory anemia, (2) low to normal leukocyte counts, (3) normal to increased platelet number with marked anisocytosis and a high proportion of megathrombocytes, (4) normal to hypoplastic erythropoiesis and generally small megakaryocytes with nonlobulated nuclei in the bone marrow. In most of the reported cases (16 out of 19) with isolated 5q-anomaly, the clinical picture and laboratory findings remained stationary during a follow-up period of up to 6 years. In only 2 out of 19 cases did acute leukemia develop. In the presence of additional chromosomal abnormalities, all the cases developed acute leukemia and especially acute myelogenous leukemia. The diagnosis of 5q-syndrome in patients with refractory anemia is of prognostic significance, since it renders possible early recognition of a potentially malignant disorder and early detection of leukemic transformation.
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PMID:[The 5q syndrome--a chromosome aberration with characteristic hematologic picture: preleukemia? Literature review and description of a personal case]. 707 78

A case of erythroid hypoplasia with refractory anemia and an interstitial deletion of the long arm of one chromosome No. 5 is described. This 5q- anomaly has been previously described in cases of refractory anemia with erythroid hypoplasia or hyperplasia, and acute myelogenous leukemia. The relationship between the 5q- chromosome and associated clinical features is discussed together with evidence against a geographical localization.
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PMID:The 5q - chromosome in a case of erythroid hypoplasia. 727 85

Activation of the N- and K-ras proto-oncogenes is the most common molecular abnormality in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). In retrospective studies, approximately 3-36% of MDS patients were reported to harbor a mutated ras proto-oncogene, with some series suggesting the presence of ras-mutations are associated with progressive disease and a poor prognosis. Since hematopoietic growth factors such as granulocyte colony-stimulating factor (G-CSF) are currently used for therapy in MDS but may stimulate the proliferation of leukemic cells, we assessed the frequency and significance of ras mutations in 27 MDS patients, 15 of whom underwent G-CSF therapy. Patients were analyzed for the presence of mutations in codons 12, 13, and 61 of the N- and K-ras proto-oncogenes. Only three patients (11%, two refractory anemia with excess of blasts (RAEB), one RAEB in transformation (RAEB-T)) harbored activated ras oncogenes with the mutations localized in N-ras codons 12 and 61. Patients were followed for periods of up to 4 years or until death supervened. Patients exhibiting ras mutations were no more likely to develop AML compared to ras-negative patients (1/3 vs. 10/24) or to have decreased survival (p = 0.64). These data indicate that, in this group of MDS patients, ras mutations do not appear to correlate with a poor prognosis, and do not adversely interact with exogenously administered G-CSF.
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PMID:Mutations in the ras proto-oncogenes in patients with myelodysplastic syndromes. 751 75

The c-mpl proto-oncogene which encodes a member of the hematopoietic cytokine receptor superfamily has been recently shown to be the receptor for thrombopoietin (TPO), which stimulates megakaryocyte progenitor expansion and differentiation. We studied c-mpl expression by Northern blot analysis, in a large series of 58 MDS. No expression was found in 14 patients with refractory anemia (RA) or with refractory anemia with ring sideroblasts (RARS). In contrast 11/26 (42%) patients with refractory anemia with excess of blasts (RAEB), or with RAEB in transformation (RAEBt), and 8/18 (44%) patients with chronic myelomonocytic leukemia (CMML) expressed c-mpl. In CMML patients, no correlation was found between c-mpl expression and any prognostic factor tested, nor with the course of the disease. In contrast, in RAEB and RAEBt, expression of c-mpl was correlated with high Bournemouth scoring (P < 0.005) and poor survival (P = 0.02) due to leukemic transformation. Forty-five per cent (5/11) of the c-mpl positive patients evolved towards AML with a mean follow-up of 10.5 months, while 13% (2/15) of the c-mpl negative patients developed a secondary leukemia, with a mean follow-up of 21.1 months. Moreover, in RAEB and RAEBt, a significant correlation was observed between c-mpl, CD34, megakaryocyte glycoprotein IIb (GPIIb) expression, and the presence of dysmegakaryopoiesis. These results indicate that patients with RAEB and RAEBt, with high expression of the c-mpl, CD34, and GPIIb genes, may identify a subgroup of patients with particularly poor prognosis, due to an increased risk of secondary leukemia. More aggressive therapy could be justified in these patients.
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PMID:Prognostic value of c-mpl expression in myelodysplastic syndromes. 753 13

We evaluated the effects of transforming growth factor-beta 1 (TGF-beta 1) on the growth of hematopoietic progenitors in normal donors and in patients with hematologic malignancies now designed as clonal disorders of multipotential stem cells. TGF-beta 1 at 80 pM exhibited differential effects on the normal hematopoietic progenitors when cells were stimulated with different growth factors, such as G-CSF, GM-CSF, interleukin-3 (IL-3), or stem cell factor (SCF). The suppressive effect by TGF-beta 1 was increased for growth with GM-CSF, IL-3, and SCF, and growth with G-CSF was unaffected in hematologic malignancies, TGF-beta 1 suppression for growth with G-CSF was increased for essential thrombocythemia (ET) and polycythemia vera; chronic myelogenous leukemia (CML) in chronic phase; CML in accelerated phase; CML in myeloid crisis; myelodysplastic syndrome (MDS) in refractory anemia; MDS in refractory anemia with an excess of blasts; and acute myeloblastic leukemia (AML). In CML-myeloid crisis and AML, TGF-beta 1 almost completely abolished the growth, with some patient-to-patient variation. The mean ED50s for the growth of leukemic blast progenitors were 1.6, 1.2, 0.7, and 0.2 pM in the presence of G-CSF, GM-CSF, IL-3, and SCF, respectively, c-myc and c-myb antisense oligonucleotides significantly suppressed the growth of leukemic blast progenitors, but not that of clonogenic cells from normal donors and patients with ET. We also demonstrated that TGF-beta 1 inhibits mRNA expression by AML blasts for c-myc and/or c-myb. When the data are taken together, growth suppression by TGF-beta 1 appears to increase with the progression of clonal evolution in hematologic malignancies.
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PMID:Differential effects of TGF-beta 1 on normal and leukemic human hematopoietic cell proliferation. 754 18

Acquired interstitial deletions of the long arm of chromosome 5, are seen in anomalies of the myeloid cells. The refractory anemia (RA) or 5q- syndrome, in which the erythroid and megakaryocytic lineages are predominantly affected, is a relatively indolent clinical entity distinguishable, from the constellation of preneoplastic myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML) with trilineage involvement. Recent molecular evidence suggests that the critical region of 5q deletion in MDS/AML resides in the D5S89 locus, which is proximal (centromeric) to the minimal region of loss in the 5q- syndrome RA. The invariable loss of the D5S89 locus in MDS/AML qualifies it for the MDS/AML tumor suppressor locus. The telomeric 5q31 gene governs erythroid and megakaryocytic differentiation and can be termed the RA locus. Isolation and characterization of these genes will lead to an understanding of molecular mechanisms underlying normal hematopoiesis and leukemic transformation.
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PMID:Molecular analysis of the 5q- chromosome. 754 26


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