Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reported a 68-year-old woman with acute nonlymphocytic leukemia, in whom the leukemia transformed from poorly differentiated myeloperoxidase (MPO)-negative type into myelomonocytic type during the observation without chemotherapy. Hematological findings on admission revealed a leukocyte count of 3,500/microliters with 48% blasts and a platelet count of 9.2 x 10(4)/microliters. Bone marrow aspiration showed 68.2% infiltration of blasts negative for MPO. Sudan black B and esterase stains. By electron microscopy MPO was detected in the endoplasmic reticulum and nucleoenvelope of the blasts. Large vacuole-like granules were MPO-negative. She was observed without administration of any antileukemic agent or an immunopotentiator. The leukocyte count rose gradually, in association with increases in the relative and absolute counts of mature neutrophils and monocytic cells, and the platelet count. Twenty-six months after the initial diagnosis, a blood examination showed a leukocyte count of 74,300/microliters with 20.5% mature neutrophils and 15.5% monocytic and a platelet count of 31.4 x 10(4)/microliters. Cytological, cytochemical, ultrastructural and immunological studies of the bone marrow cells showed features compatible with acute myelomonocytic leukemia (FAB M4). This case is unusual in respect that poorly differentiated ANLL transformed spontaneously into moderately differentiated ANLL.
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PMID:[Spontaneous differentiation from myeloperoxidase-negative acute nonlymphocytic leukemia to acute myelomonocytic leukemia]. 255 92

Murine myelogenous leukemias can be classified into several distinct subgroups based on morphology, cytochemical staining, and immunoreactivity. The leukemias invariably involve the spleen and the extent of infiltration into other tissues is variable. The myelogenous nature of the leukemia is readily apparent in well-differentiated leukemias on the basis of morphology; with poorly differentiated leukemias, positive staining with chloroacetate esterase, nonspecific esterase, and certain monoclonal antibodies such as Mac-1, is helpful to establish myelogenous differentiation. Subgrouping of myelogenous leukemias depends on the presence or absence of monocytic differentiation, as ascertained by staining with Mac-2, electron microscopy or phagocytosis. Leukemias showing no monocytic differentiation can be classified as myeloblastic, corresponding to the FAB M1 and M2 subtypes in humans. Leukemias exhibiting both monocytic and granulocytic features are myelomonocytic, corresponding to the FAB M4 subtype. Tumors with only monocyte differentiation arise primarily as solid tumors in mice, and a leukemic phase is variable.
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PMID:The pathology of murine myelogenous leukemias. 265 81

The serum concentration of LDH increases in various cancers and its increase can represent a prognostic marker of the disease and a good indicator of the tumoral mass's degree of growth. In patients with acute leukaemia, LDH can show a moderate increase only in some cases of acute non-lymphoblastic leukaemia with FAB M4 and M5 cytotype, whereas in acute lymphoblastic leukaemia LDH almost always increases, an event related to the number of white cells during remission or a relapse of the disease. In non-Hodgkin lymphomas, measurement of total LDH is not on its own a useful aid for monitoring the therapeutic response and the course of the disease. In such cases it is right to also evaluate LDH isoenzymes because they pinpoint the persistence of residual lymphomatous foci which do not affect the level of total LDH and have not clinical evidence.
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PMID:[Clinical significance of the determination of lactate dehydrogenase in acute leukemia and non-Hodgkin's lymphoma]. 274 83

This thesis is a survey of nine previously published articles on MPO deficient PMN. The incidences in leukaemia and allied disorders of the presence of this abnormal subpopulation of mature neutrophils and the relationship to clinical course in AML, susceptibility to infections in AML, FAB classification in AML and MDS, cytogenetically defined aberrations in MDS and morphometrical characteristics were investigated. The aims of the studies were to examine the diagnostic as well as the prognostic value of the parameter, to examine the usefulness of the parameter as an predictive indicator of CR and relapse in AML and to examine the concept that MPO deficient PMN may originate from leukaemic precursors. MPO deficient PMN were found to occur in a minor number (less than 4% of the total number of PMN) in normal humans and the incidences of an abnormal number (greater than 4%) were found to be about 40% in AML (I, II, III, IV, VIII), 60% in CML (I, VII), 30% in MPD other than CML (VII) and 30% in MDS (V). The highest incidences in AML were found in the FAB subtypes possessing the most myeloid differentiation potential i.e. FAB M2 and FAB M4 (IV). In ALL, CLL, HCL, Hodgkin's disease, anaemia not related to leukaemia and leukaemoid reactions the incidences all were 0% (I, unpublished data). The abnormal MPO deficient PMN subpopulation, if present, disappeared when CR was achieved and reappeared when relapse eventually was developed (II, VIII). In both situations serial determinations showed that the change occurred before the usual routine blood examinations predicted CR and relapse; several days and several months prior, respectively (VIII). The probability of obtaining CR was lower in the AML patients with the abnormal subpopulation and the risk of developing relapse higher than in AML patients without the anomaly (II, VIII). These differences were not statistically significant, however. AML patients, showing an increased number of MPO deficient PMN, revealed a statistically significant increased susceptibility to infections (P less than 0.01) during the preremission phase accounting for 18% to 67% of the total number of infections in this period (III). This increase was positively correlated to the extent of the anomaly (P less than 0.002). The spontaneous occurrence of a subpopulation of MPO deficient PMN in MDS went together with a simultaneous progression in cytogenetically determined clonal chromosomal aberrations and were related to progression in FAB subtype as well (VI). Morphometrically MPO deficient PMN were characterized by a decreased total cell size and an increased nucleus size of the projected images (IX).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Myeloperoxidase deficient polymorphonuclear leucocytes in leukaemia and allied disorders. 285 15

Simultaneous involvement of bands 8p11 and 16p13 in a primary, even though rare, chromosomal translocation recently described in acute nonlymphocytic leukemia may be of crucial interest in some subtypes of this acute leukemia, particularly in the monocytic form. In the present report we describe this translocation in acute nonlymphoblastic leukemia FAB M4, possibly secondary to Hodgkin's disease, though it is also possible that the leukemia may have developed de novo. The aberration t(8;16)(p11;p13) was present in 100% of direct and cultured bone marrow cell preparations. A very high frequency of cells with nonclonal structural chromosome aberrations was also observed in peripheral blood cultures (more than 53%). Random translocations and deletions constituted most of the observed alterations. These findings are discussed with regard to the relationships between secondary leukemias and intensive polychemotherapeutic treatments of primary neoplasias.
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PMID:Translocation t(8;16)(p11;p13) in acute nonlymphoblastic leukemia (M4) possibly secondary to Hodgkin's disease. 291 27

The cellular origin of acute undifferentiated leukemia (AUL) is still a matter of controversy. We report on two cases in which the diagnosis of AUL was established according to restricted criteria. Blast cells of both patients showed phenotypic conversion during the course of disease. In one case, within 24 days from starting treatment, the leukemic phenotype changed from AUL to acute myelomonocytic leukemia (FAB L1, TdT+ to FAB M4, TdT-). The initial phenotype of this acute leukemia was characterized by the co-expression of both B-lymphoid and myeloid markers on the same cell. Moreover, analysis of esterase isoenzyme pattern showed the whole spectrum of isoenzymes typically seen in myelomonocytic leukemias already at diagnosis, yet blast cells additionally contained all three isoenzymes of beta-hexosaminidase typically seen in AUL. However, examination of immunoglobulin (Ig) heavy chain gene rearrangement initially and after conversion revealed an identical monoclonal configuration of Ig heavy chain sequences in both samples. The second AUL patient relapsed after allogeneic bone marrow transplantation with common ALL-antigen (CALLA) positive acute leukemia. Subsequent Southern blot analysis showed a novel rearranged Ig fragment compared to the analysis before transplantation indicating that the leukemic clones prior to and after transplantation were not identical. No chromosomal abnormalities were observed in both cases. These data support the view that AUL cells originate from a pluripotent stem cell that is capable to differentiate in the myelomonocytic lineage (patient 1), and confirm the value of Ig gene analysis as marker for cellular clonality.
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PMID:Conversion of acute undifferentiated leukemia phenotypes: analysis of clonal development. 294 79

A case of severe cutaneous haemorrhage due to thrombocytopenia in combination with an acquired haemophilia A is reported. The thrombocytopenia was due to acute myelomonocytic leukaemia (FAB M4). A factor VIII:C specific anticoagulant was also found. Chemotherapy led to complete remission with normal blood counts and coagulation-test results.
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PMID:Acute myelomonocytic leukaemia and acquired haemophilia A with severe cutaneous haemorrhage. 309 35

The leukemic blasts of 22 patients with acute myelocytic and myelomonocytic leukemia were tested by indirect immunofluorescence with the monoclonal antibodies BL-DR (directed against HLA-DR-antigens), BL-M/G (react with both granulocytes and monocytes), BL-T2 (pan-T-lymphocyte-antibody CD 5), and BL-Ig-L/1 (anti-light-chains-antibody). The leukemic blasts showed no crossreaction with BL-DR and BL-Ig-L/1. Both the antibodies BL-DR and BL-M/G reacted mainly with the acute myelomonocytic leukemias FAB M4 and only seldom with the acute myelocytic leukemias FAB M1, M2, and M3. The antibodies BL-DR and BL-M/G are able to confirm the diagnosis of acute myelomonocytic leukemia and to classify some previously unclassifiable leukemias.
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PMID:[Testing of acute myeloid leukemia of humans using monoclonal antibodies BL-DR, BL-M/G, BL-T2 and BL-Ig-L/1]. 313 13

PMN elastase is a useful additional parameter in the differential diagnosis of the leukaemias. In all patients with myelocytic leukaemias there were elevated levels of elastase-alpha 1-proteinase inhibitor (E-alpha 1PI), while in the lymphatic leukaemias complexed elastase levels were decreased. The highest values were found in the peripheral blood plasma and bone marrow plasma of patients with CML. Despite high E-alpha 1PI concentrations there were no signs of bleeding or consumption of plasmatic coagulation factors. In AML a wide range of E-alpha 1PI levels was observed, extending from slightly elevated to four hundred-fold increased. In myeloblastic leukaemias without maturation (FAB M 1) the concentrations of complexed elastase remained below 150 ng/ml. In myeloblastic leukaemias with maturation (FAB M2) the E-alpha 1PI values ranged between 214 ng/ml and 850 ng/ml (means = 402 +/- 69), and in myelo-monoblastic leukaemias (FAB M4) between 450 ng/ml and 720 ng/ml (means = 663 +/- 72). The only case of promyelocytic leukaemia (FAB M 3) exhibited an extremely high value of 4,550 ng/ml, while a monocytic leukaemia (FAB M5) showed an extremely low value of 5 ng/ml. During cytostatic therapy there was a rapid decrease in levels of complexed elastase, with E-alpha 1PI values returning to normal in remission. In recidivating cases there was an increase of E-alpha 1PI levels in AML and a decrease in ALL. There was a correlation between the E-alpha 1PI concentrations in peripheral plasma and leukaemic bone marrow infiltration, so providing a good basis for monitoring remission from leukaemia and indicating relapse. It was also interesting to observe an extremely low E-alpha 1PI level (5 ng/ml) in patients with myelodysplasia. Under Decortin/Plenastril therapy the concentration rose to 50 ng/ml. An E-alpha 1PI level of 10 ng per ml was observed in one case of Ranitidine agranulocytosis. Under corticoid therapy the value returned to normal within eight days.
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PMID:The importance of granulocyte elastase in haematological diagnosis. 316 79

Nineteen patients with inv(16)(p13q22) or del(16) in myeloid leukemia are described. Eight showed inv(16)(p13q22), including one with de novo acute myeloid leukemia (AML-M2) and seven with de novo acute myelomonocytic leukemia (AMML-M4). Additional chromosome changes were detected in five of the cases; the most common change was trisomy 22. All but one of the de novo M2 and M4 leukemia patients with inv(16)(p13q22) showed initial bone marrow eosinophilia (greater than 5%) with basophilic granules. The remaining 11 showed deletion of the long arm of a chromosome no. 16 [del(16)(q22 or q23)]. Eight of the 11 were diagnosed as having chronic myelomonocytic leukemia, three transformed into an acute phase with M4 morphology; none of them gained complete remission. Two of the remaining three patients with del(16) were diagnosed as having M4 leukemia without marrow eosinophilia. The remaining one was a case of M4 leukemia following a myelodysplastic syndrome. The findings indicate that del(16) might be related to chronic myelomonocytic leukemia or leukemia with a prior history of myelodysplastic syndrome without evidence of marrow eosinophilia. On the other hand, inv(16)(p13q22) is highly associated with de novo AML especially AMML-M4 with bone marrow eosinophilia and a favorable prognosis.
Leukemia 1988 Jan
PMID:Chromosome change at 16q22 in nonlymphocytic leukemia: clinical implication on leukemia patients with inv(16) versus del(16). 342 28


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