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)

From 1980 to 1987, three cases of chronic myelomonocytic leukemia (CMML) were encountered among 68 cases of multiple myeloma who survived more than three years from the diagnosis. The incidence (4.8%) of secondary myelodysplastic syndrome (MDS) is almost identical to previous reports, but case reports of chronic myelomonocytic leukemia were rare. In Japan, there are few reports of multiple myeloma patients who later developed secondary MDS or acute myelogenous leukemia (AML). In our cases, none of the 31 patients treated with cyclophosphamide developed secondary MDS, while three of 37 patients treated with melphalan developed CMML. This difference is not statistically significant.
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PMID:Three cases of multiple myeloma developing into melphalan-related chronic myelomonocytic leukemia. 177 Mar 23

A 9-month-old boy with known familial neurofibromatosis type I (NF-1) presented with a clinical and laboratory picture suggestive of juvenile chronic myelomonocytic leukemia (JCMMoL). Chromosomal studies obtained from the bone marrow indicated, however, that he had monosomy 7 syndrome. We believe this is the first reported case of monosomy 7 syndrome in a child with NF in the United States, and that this case complements a recent report of two cases of NF, JCMMoL, and monosomy 7 in Japanese children. Since monosomy 7 syndrome is very difficult to differentiate from JCMMoL or acute nonlymphocytic leukemia (ANLL) unless appropriate chromosomal studies are obtained, we believe it is possible that monosomy 7 may occur with increased frequency in patients with NF-1. Monosomy 7 syndrome might therefore be a significant cause of the known association between NF-1 and nonlymphoid leukemia.
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PMID:Monosomy 7 syndrome in an infant with neurofibromatosis. 179 61

The prognostic value of the FAB classification, bone marrow histology, Bournemouth score, and chromosome findings was studied in 88 patients with primary myelodysplastic syndromes. The median survival for the whole group of patients was 22 months (RA 61.7 months, RARS 31.6 months, CMML 15.7 months, RAEB 10.3 months, and RAEBt 8.2 months). Chromosomal abnormalities were found in 37 of the 70 patients investigated (52%). Only the differences in survival between patients with complex versus normal karyotype were statistically significant (p = 0.02). The presence of small blastic cells, located away from the endosteal surface (abnormal localization of immature blasts or ALIP) appears to be a major prognostic factor in predicting the duration of survival and progression to ANLL, especially in the FAB subgroups RA and RARS. Median survival for the 22 ALIP- cases with RA/RARS was 65 months, compared with 31 months for the ALIP+ cases (p = 0.0006). Nine ALIP+ patients (53%) developed ANLL in contrast to 3 (13%) of the ALIP- cases (p = 0.008). By redefining ALIP and evaluating the number and characteristics of the accompanying cells, histological subtypes were distinguished correlating largely with the FAB subgroups. Our findings demonstrate the prognostic importance of bone marrow biopsy and quantifying the complexity of bone marrow chromosome changes. It should be helpful in evaluating current attempts to find effective treatment for patients with MDS.
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PMID:Update on the prognostic implication of morphology, histology, and karyotype in primary myelodysplastic syndromes. 179 66

Nonrandom cytogenetic abnormalities have been described in a variety of human malignancies including myelodysplastic syndromes (MDS). Acquisition of new chromosomal abnormalities may herald onset of a more aggressive disease. We report a patient with chronic myelomonocytic leukemia (CMMoL) who initially had a normal karyotype, but in whom the clonal interstitial deletion of chromosome 15 (q11-q15) was coincident with development of acute myeloid leukemia (AML) one year later. To date, this chromosomal change has not been reported in CMMoL, AML, or any other human malignancy.
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PMID:del(15)(q11q15) associated with transformation of chronic myelomonocytic leukemia. 191 5

Bryostatin 1 is a macrocyclic lactone which activates protein kinase C (PKC), and is able to induce maturation in cells from some cases of acute myelogenous leukemia. This paper reports that bryostatin inhibits the spontaneous in vitro proliferation of chronic myelomonocytic leukemia cells (CMMoL) in semi-solid medium at concentrations between 10(-8) and 10(-10) M. Growth inhibition was equivalent to or greater than that seen with phorbol-12-myristate-13-acetate. Bryostatin acted primarily as a cytotoxic agent, rather than as a cytostatic agent. The spontaneous in vitro proliferation of CMMoL cells is due to autocrine or paracrine secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF). Bryostatin 1 actually increased GM-CSF secretion by CMMoL cells while inhibiting their proliferation. Bryostatin 1 also increased tumor necrosis factor alpha (TNF alpha) secretion by CMMoL cells, and in 2/5 cases the cytotoxic effect of bryostatin 1 on fresh CMMoL cells could be substantially reversed by the addition of antibody to TNF alpha to the culture medium. Bryostatin 1 may produce a cytotoxic effect on CMMoL cells in part by increasing the secretion of, or sensitivity to, TNF alpha, and may have therapeutic potential in CMMoL.
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PMID:Bryostatin 1: a potential anti-leukemic agent for chronic myelomonocytic leukemia. 202 97

Interleukin-3 (IL-3) is a T-cell-derived colony-stimulating factor (CSF) whose primary targets include relatively early, multipotential, hematopoietic progenitor cells. In this trial, we treated 24 patients with recombinant human IL-3 given by a daily 4-hour intravenous infusion for 28 days. The dose levels were 30, 60, 125, 250, 500, 750, and 1,000 micrograms/m2/d. At least three patients were entered at every dose level. Each participant suffered from bone marrow failure, with the underlying diagnosis being myelodysplastic syndrome (13 patients), aplastic anemia (eight patients), or aplasia after prolonged high-dose chemotherapy (three patients) for multiple myeloma, breast cancer, or acute myelogenous leukemia. Most patients tolerated therapy well, with the most frequent side effects being low-grade fever and headaches. Hematopoietic changes included modest increases in neutrophil counts (eight patients), eosinophil counts (six patients), platelet counts (three patients), and reticulocyte counts (two patients). An increase in blasts occurred in one patient who had refractory anemia with excess blasts in transformation and was reversible once IL-3 was discontinued. In addition, one patient with chronic myelomonocytic leukemia showed an increase in monocytes (and granulocytes). Progression to acute leukemia did not occur. Pharmacokinetic analyses showed a rapid clearance with a mean half-life of 18.8 minutes at the 60 micrograms/m2/d dose, and 52.9 minutes at the 250 micrograms/m2/d dose. Serum concentrations of 10 to 20 ng/mL of IL-3 were achievable at the 250 micrograms/m2/d dose. Our observations indicate that recombinant human IL-3 can be given safely at doses of 1,000 micrograms/m2/d or less. In addition, on the basis of preclinical data and the biologic activity observed in this study, further trials of this molecule, alone and in combination with other growth factors, are warranted in patients with pancytopenia.
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PMID:Phase I study of recombinant human interleukin-3 in patients with bone marrow failure. 204 65

We performed Southern blot analysis of the p53 gene in 62 patients (37 de novo myelodysplastic syndromes (MDS), of which 10 were studied after progression to acute myeloid leukemia (AML); 14 MDS secondary to chemo or radiotherapy; 11 de novo AML). Thirteen of the 56 patients studied cytogenetically had monosomy for the short arm of chromosome 17 and, in another patient who had secondary MDS, a translocation involving a breakpoint in 17p13 where the p53 gene was mapped was found. This patient was the only individual in whom a rearrangement of p53 DNA was seen. Sixteen of the 62 patients were studied by Northern analysis, and reduced or undetectable 2.8 kb p53 transcript was found in 6 of them, who had predominantly monosomy for 17p or chronic myelomonocytic leukemia. Rearrangements of the 53 gene, identifiable by Southern analysis, are a rare finding in patients with MDS and AML, even in those with monosomy for 17p, but reduced expression of the p53 gene is relatively common. We are currently trying to detect point mutations of the p53 gene by PCR technology especially in patients with monosomy for 17p.
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PMID:Rearrangement and expression of the p53 gene in myelodysplastic syndrome and acute myeloid leukemia. 209 8

Normal and leukemic hematopoietic cell lysates were labeled with [3H]-diisopropylfluorosorophosphate ([3H]-DFP), an active site inhibitor of serine hydrolases. The labeled proteins in the lysates were examined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by counting of gel segments for radioactivity. The results indicate the presence of distinct [3H]-DFP binding patterns for different normal and leukemic hematopoietic cells; significantly lower labeling in normal or leukemic lymphoid cells compared to myeloid or monocytoid cells; lower labeling in acute myeloblastic leukemia (FAB-M1) as compared to acute myelomonocytic leukemia (FAB-M4), chronic myelomonocytic leukemia or monocytes and an increase in [3H]-DFP binding with cell maturation along granulocytic series. Thus, these patterns could be useful in discriminating acute lymphoblastic leukemia from myeloid/monocytoid types of leukemia and for following maturation of myeloid cells, and perhaps for studying functional or maturation defects in hematopoietic cells in other pathological conditions.
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PMID:Diisopropylfluorophosphate binding proteins (serine hydrolases) from normal and leukemic hematopoietic cells. 211 31

As part of a multicenter trial 12 patients with myelodysplastic syndromes (MDS) were treated with 14-day-cycles of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF; 250 micrograms/m2 day s.c.). In addition, all patients received 20 mg/m2/day s.c. cytosine-arabinoside (Ara-C) 12 h after GM-CSF except for patients suffering from refractory anemia (RA) according to FAB classification. Courses were repeated after 4 weeks. In 11 evaluable patients, results according to FAB-classified MDS were as follows: RA, 1/2 response (R), 1/2 stable disease (SD); RAEB, 2/3 R, 1/3 SD; RAEB-T, 1/6 CR, 1/6 PR, 2/6 R, 2/6 progression; CMML, 1/2 SD. In 2 patients with RAEB-T, overt acute myeloid leukemia was observed 2 and 10 weeks after initiation of treatment. With few exceptions, treatment resulted in a prompt increase in granulocytes and eosinophiles. This was associated with improvement of infectious complications. Increases in red cells and platelets occurred variably and was apparently associated with responses of the underlying disease. Dose limiting side effects consisted of fever, severe fatigue and dolent local reactions at the site of GM-CSF injection. In addition, nausea and diarrhoea occurred frequently. Less often, respiratory and cardiovascular side effects were encountered. In summary, GM-CSF +/- Ara-C in MDS results in objective remission with manageable toxicity. Conceivably, this regimen will serve as a base for future treatment strategies against MDS.
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PMID:Recombinant human granulocyte-macrophage colony-stimulating factor and low-dose cytosine-arabinoside in the treatment of patients with myelodysplastic syndromes. A phase II study. 218 22

We studied the expression of IL 6 gene in 49 patients, including 21 chronic myelomonocytic leukemias (CML), 9 other myelodysplastic syndromes (MDS), 18 acute myeloid leukemias (11 M2 or M3 and 7 M4 or M5) and 1 case of acute biphenotypic lymphoid monocytic leukemia. IL 6 was found expressed only in the latter patient and in one patient with M5 acute myeloid leukemia. DNA analysis by Southern blot revealed no rearrangement in these 2 patients and in 10 of the other patients who showed no IL 6 expression. These results do not support an autocrine role for IL 6 in CMML or in other MDS. In acute myeloid leukemias, if expressed by leukemic cells, IL 6 seems to be restricted to cases with a monocytic component, although the number of patients was too small to draw any definite conclusion.
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PMID:Expression of the interleukin 6 gene in acute myeloid leukemia and myelodysplastic syndromes: a report on 49 cases. 221


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