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

Of particular interest in the study of cell membrane markers of leukemic cells were cytotoxic and immunofluorescent results obtained in comparing Ia alloantigen and complement receptor (CR) expression on normal leukocytic and leukemic cell types. Using discontinuous Ficoll gradients, Ia alloantigens were found on varying numbers of leukemic myelo- and lymphoblasts, and on the early stages of normal melocytes. Ia alloantigens, however, were not detectable on mature polymorphonuclear cells. This establishes human Ia alloantigens as cell surface differentiation markers. The appearance of complement receptors was observed later than that of Ia alloantigens. CR1 (EAC1-4b) showed up later in the differentiation than CR2 (EAC1-3d). Thus, an immunological discrimination between AML blasts and CML blast crisis blasts appears to be possible: AML blasts are mostly Ia-positive but CR-negative, whilst CML blast crisis cells are only 20-30% Ia-positive and carry complement receptors in at least equal amounts. The AML blast cell would appear as the less-differentiated cell type when compared to the CML blast crisis cells. The picture, however, remains complex since in CML blast crisis at least three different types of blast cells can be identified: an Ia-positive and an Ia-negative myeloid blast as well as an Ia-positive lymphoid blast. The quantitative composition of these three elements within the myeloid differentiation profile can vary somewhat from patient to patient. Furthermore, these studies revealed a disturbed differentiation of leukemic cell types.
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PMID:Classification of leukemic cells by Ia alloantigens and complement receptors. Surface probes for cell differentiation. 37 3

Of three patients with mediastinal malignant lymphoma, lymphoblastic type, at the time of diagnosis one also had acute myeloblastic leukemia (AML), and the other two had blood and bone marrow findings indicative of acute lymphoblastic leukemia (ALL). The latter two patients developed the hematologic picture of AML less than eight months later. In all cases, AML was confirmed by cytochemical studies of peripheral blood and bone marrow cells. Autopsy of two of the patients revealed only AML. The myeloid nature of the proliferative cells was demonstrated with the naphthol-ASD-chloroacetate stain (NCA) on postmortem tissue sections. This study further supports the hypothesis of a common origin of neoplastic lymphoid and myeloid cells from pluripotent bone marrow stem cells.
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PMID:Acute myeloblastic leukemia developing in patients with mediastinal lymphoblastic lymphoma. 38 13

Fourteen cases of philadelphia chromosome (Ph1) positive chronic myeloid leukaemia in blast transformation have been investigated using cell surface markers. Morphologically eight cases were lymphoid and the remainder myeloid in appearance. All cases were negative with surface markers for thymocytes and T and B lymphocytes. Five of the lymphoid cases reacted with an antiserum specific for acute lymphoid leukaemia )ALL) of non-T non-B type and were also weakly reactive with a lymphocyte reactive antiserum. A sixth patient, whose blast cells were anti-ALL negative (ALL-) at presentation, subsequently developed central nervous system leukaemia with anti-ALL positive (ALL+) blast cells in the CSF. In all cases the leukaemic blast cells showed greatly diminished expression of cholera toxin receptors when compared to granulocytic cells from the chronic phase of CML. This parallels weak or negligible expression of the cholera toxin receptor in ALL and AML. These results suggest that the blastic phase of CML may involve different cellular derivatives of a pluripotential stem cell in which the primary malignant/genetic changes reside. The blast crisis of CML can therefore be heterogeneous with respect to cellular expression and in a significant proportion of patients involves a cell which is by membrane markers and morphological criteria indistinguishable from that seen in the common form of ALL. In these cases the Philadelphia chromosome may be the only distinguishing cellular characteristic.
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PMID:Blast crisis of chronic myeloid leukaemia (CML). II. Cell surface marker analysis of "lymphoid" and myeloid cases. 78 72

Chromosome analyses using the Giemsa banding technique were performed on bone marrow cells in a patient with the association of Hodgkin's disease and acute myeloid leukaemia. All cells had an abnormal karyotype showing an extra chromosome No. 14, loss of one chromosome No. 17 and gain of one chromosome No. 18. These abnormalities are in many respects similar to the karyotype changes of lymphoid cells in malignant lymphomas, suggesting a pathogenetic relationship between the two disorders.
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PMID:Chromosome abnormalities identified by banding technique in a patient with acute myeloid leukaemia complicating Hodgkin's disease. 105 40

From May 1985 to June 1990, 94 newly diagnosed cases of acute myelogenous leukemia (AML) were treated at the Institut Gustave-Roussy, of which four (4.3%) demonstrated mixed cell lineage. All these cases were morphologically and cytochemically considered as myelogenous leukemias according to the FAB classification. Immunophenotyping revealed in all four cases that the blast population had T-lymphoid (CD2, CD5, CD7 and cytoplasmic CD3) markers. In three of these cases, blast cells co-expressed myelogenous CD13 and CD33 markers. Cytogenetic analysis of the blast cells revealed a normal karyotype in all cases. The response to therapy has been poor. The two patients initially treated with a regimen usually used for AML did not achieve complete remission. By contrast, in three cases, complete remission was obtained with a drug combination used for lymphoblastic leukemia (in one case after failure of first line AML regimen). Only one patient remained disease-free for more than 18 months. We conclude that this form of leukemia is a distinct biological and clinical entity and may benefit form alternative therapy.
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PMID:Acute myelogenous leukemia with T-cell features. 130 36

The enzyme myeloperoxidase (MPO) is the hallmark of the myeloid lineage. We have analysed the presence of MPO in blasts from 180 cases of acute leukaemia (103 acute myeloid leukaemia (AML) and 77 acute lymphoid leukaemia (ALL) by means of monoclonal antibodies anti-MPO and immunocytochemistry (alkaline phosphatase anti-alkaline phosphatase method). The aim of the study was to investigate the specificity and sensitivity of this marker compared with MPO cytochemistry by light (LM) and electron microscopy (EM), and with the expression of myeloid antigens. Anti-MPO was positive (greater than 3% blasts) in all but one of the 90 AML positive by LM cytochemistry. Of 13 AML cases negative by MPO cytochemistry, six showed 3-10% blasts reactive with anti-MPO and were also positive with antibodies to CD13 and/or CD33. The presence of MPO was confirmed in four of these by EM. The overall positivity of anti-MPO in AML was 92%. Anti-MPO was negative in all but two ALL (6% and 8% positive blasts). The blasts in these two cases were also CD13, CD33 and MPO positive by EM; both were thus reclassified as biphenotypic. Another two ALL reinterpreted as biphenotypic were negative by MPO cytochemistry and anti-MPO but were MPO positive by EM and with CD13 and/or CD33. We conclude that anti-MPO is a sensitive and specific early marker of myeloid blasts and should be incorporated in the routine immunophenotyping of acute leukaemia.
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PMID:The role of an anti-myeloperoxidase antibody in the diagnosis and classification of acute leukaemia: a comparison with light and electron microscopy cytochemistry. 131 Nov 96

The immunophenotype of leukaemia cells from 60 patients with acute myeloid leukaemia (AML) was analysed with the APAAP technique using a panel of anti-myeloid and lymphoid associated monoclonal antibodies (McAb). Cells from all cases, including three with negative cytochemical features, were labelled by at least one of the anti-myeloid McAb CD13, anti-myeloperoxidase (anti-Mpo), and/or CD14. The most sensitive marker was CD13, since it was positive in 90% of cases. In two out of three AML cases defined as M0-AML, CD13 was expressed in the cytoplasm but not on the membrane; in these three cases peroxidase (Mpo) was not detected by conventional cytochemistry, but could be demonstrated in all of them using the McAb anti-Mpo. The simultaneous expression of CD14 and CD68 McAb was often confined to the M4 and M5 FAB AML subtypes (92% cases) as compared to the others: M1, M2, M3 (18% cases). Lymphoid antigens were rarely positive (TdT+: 13%, CD7+: 15%, CD19+: 5%) and none of the AML cases were CD3+ or CD10+. By contrast, CD4 was expressed in blasts from 44% of cases and this was not restricted to AML with a monocytic component (M4, M5) but also found in other subtypes. There were no significant differences in the clinical or prognostic features according to the positivity or negativity with TdT and CD4. By contrast, expression of CD7 was associated with refractoriness to the treatment or short complete remission duration, although the number of patients is too small to draw firm conclusions. Our findings support the clinical and diagnostic relevance of immunophenotypic studies in AML.
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PMID:The value of detecting surface and cytoplasmic antigens in acute myeloid leukaemia. 132 89

Philadelphia chromosome (Ph') was detected at presentation in 10 out of 110 patients with acute lymphoblastic leukemia (ALL) and five of 168 patients with acute myelogenous leukemia (AML). Two other ALL patients who had studies at relapse were also included in the analyses. One of the 12 Ph'-positive (Ph+) ALL patients had simultaneous expression of myeloid-associated antigen on the leukemic blasts, while all the five AML patients coexpressed markers of lymphoid cells. Double labeling of the cells with myeloperoxidase and CD10 on three Ph+ AML cases showed that most leukemic blasts expressed either myeloperoxidase activity or CD10 but not both. Cross-lineage gene rearrangements of T-cell receptor (TCR) beta-chain gene were detected in three of the eight Ph+ ALL patients tested. All the four Ph+ AML cases studied showed immunoglobulin heavy chain gene rearrangements, and three of them also had simultaneous rearrangements of TCR beta-chain gene. The results revealed that Ph+ acute leukemia in this study belonged either to ALL or mixed lineage leukemia, and none was pure AML. This finding is contrary to that of acute blast crisis of chronic myelogenous leukemia in which the majority of patients had myeloid transformation. Rearrangements of bcr were detected in four of the 10 Ph+ ALL and three of the four Ph+ AML patients tested. No significant difference was noted in the clinical or hematologic manifestations among Ph+ leukemia with or without bcr rearrangements.
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PMID:Characterization of Philadelphia-chromosome-positive acute leukemia by clinical, immunocytochemical, and gene analysis. 132 82

Myeloperoxidase (MPO)- and Sudan Black B-not more than 3%-positive, esterase staining-negative, lymphoid, megakaryocyte lineage and erythroid surface marker-negative and electron microscopic platelet peroxidase-negative acute leukemia (AL) was diagnosed as acute undifferentiated leukemia (AUL), and myeloid marker (CD13, CD33), electron microscopic MPO (EMMPO), and DNA analysis of immunoglobulin heavy chain and T cell receptor as well as chemotherapy and its reactivity were examined. Of 239 cases of AL, 10 (4.2%) were AUL, and of these 10 cases, 9 were CD13 or CD33-positive AML-MO (MO) cases. Of 9 cases examined for EMMPO, 4 (44%) were positive, and of 3 cases of MO subjected to DNA analysis, 1 and 1 showed rearrangements of immunoglobulin heavy chain and T cell receptor beta chain, respectively. Of 6 cases of MO on myeloid induction therapy, 1 and 1 showed complete remission (CR) and partial remission (PR), respectively, each having lymphoid genotype, and 4 showed no remission (NR), being 3 of them EMMPO-positive. Of 2 cases on lymphoid induction therapy, 1 and 1 showed CR and NR, respectively, the former being EMMPO-positive MO. BHAC-EM therapy with behenoyl cytosine arabinoside, VP-16 and mitoxantrone performed on 2 cases refractory to any one of both these myeloid and lymphoid induction therapies led to CR in all these 2 cases.
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PMID:[Acute undifferentiated leukemia from the viewpoints of diagnosis and therapy]. 133 62

In order to investigate the role of T-cell receptor (TcR)-delta and TcR-gamma gene rearrangements and/or deletions in acute myeloid leukemia (AML) coexpressing T-cell-associated antigens (i.e. CD2 and/or CD4 and/or CD7), we examined blasts from a selected group of 56 AML cases (25 children, 31 adults) coexpressing either of these antigens without cytoplasmic CD3 expression. Forty-four typical AML cases (7 children, 37 adults) without T-cell associated antigens were further studied as controls. Germline configuration of the TcR-delta gene was observed in 91 out of the total of 100 AML cases investigated. Eight of nine cases with rearranged or deleted TcR-delta genes coexpressed T-cell-associated antigens. Blast cells of 7/9 cases were classified as FAB M1, two as FAB M2. In six of these cases TcR-gamma gene rearrangements were also detected. TcR-delta alterations were predominantly found in children whose blasts coexpressed T-lymphoid associated antigens (6/25, 24%), but were rarely detected in adult AML with or without coexpression of T-cell antigens (2/31 and 0/37, respectively).
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PMID:Rearrangements of T-cell receptor delta, gamma and beta genes in acute myeloid leukemia coexpressing T-lymphoid features. 133 55


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