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

Leukemic cells from 21 to 197 adult patients with de novo acute myelocytic leukemia (AML) were positive for IL-2R alpha chain (IL-2R alpha), whereas IL-2R beta chain (IL-2R beta), which is responsible for IL-2 signal transduction, was not found on leukemic cells from any of these cases tested. The expression of IL-2R alpha was closely associated with that of adhesion molecules CD4, CD11b and CD22, and endopeptidase CD10. None of the IL-2R alpha (+) AML cells responded to recombinant human IL-2. These data suggest that IL-2R alpha on AML cells may not be involved in cellular proliferation as one of growth factor receptors but may have a role in the control of cell-to-cell interactions.
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PMID:Interleukin-2 receptor alpha chain on acute myelocytic leukemia cells is involved in cell-to-cell interactions. 842 75

This report describes 4 cases of T-cell-associated CD7-positive acute myeloid leukemia (AML). Myelo-peroxidase staining of blasts was negative in 2 cases but became positive during their courses. In all cases, the myeloid determinants CD13 and/or CD33 were associated with CD7 expression. Other B-lymphoid (CD10, CD19) or T-lymphoid (CD2) markers were negative. In three cases, dual fluorescence analyses showed co-expression of CD7 and CD13 (CD33). Clinically, compared with CD7+AML, these CD7+AML patients presented higher leukocyte and blast counts in peripheral blood. All patients achieved complete remission with chemotherapeutic regimens for AML, but 3 relapsed within a short time. Systemic lymphadenopathy was found in 2 cases, and interestingly, the surface markers of the lymph-node in one case were CD7+CD33-. These cases of CD7+AML may represent a distinct subgroup that arises from particular, less different myeloid precursors, and may have poor prognosis.
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PMID:[Four cases of CD7-positive acute myeloid leukemia]. 845 Jun 9

The clinical and biologic characteristics of acute myeloid leukemia (AML) with coexpression of lymphoid-associated antigens (Lym+ AML) were studied from 39 cases who represented 24% of 161 newly diagnosed de novo AML. Twenty-seven cases (16.8%) were positive for the expression of T-cell markers (T+ AML) and 12 (7.5%) for B-cell markers (B+ AML). Chromosomal abnormalities t(9;22)(q34;q11) and t/del(11)(q23), which were considered to be associated with acute leukemia coexpressing markers of more than one cell lineage, were detected in five and in four patients, respectively. There was no prognostic significance of B-cell or T-cell antigen expression in AML. Of 12 T+ AML cases in which cells were available for gene analysis, all showed germline configuration of immunoglobulin heavy chain and T-cell receptor beta chain genes, while seven of nine B+ AML showed rearrangements of either or both of the genes. Double labeling of the cells with myeloperoxidase and lymphoid markers demonstrated that individual blasts in all the five T+ AML tested were simultaneously expressing myeloperoxidase activity and CD7; however, most blasts in the three B+ AML studied expressed either myeloperoxidase activity or CD10, but not both. In eight of the nine T+ AML tested, the T-cell antigen-positive leukemic blasts were significantly decreased to less than 10%, after in vitro culture with the differentiation-inducing agent phorbol ester. B-cell markers remained positive (> or = 20%) on the cells in the two B+ AML who had the same study. These findings suggested that T+ AML and B+ AML might have different biologic features. Further studies on more patients are needed to clarify this point.
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PMID:Characterization of acute myeloid leukemia (AML) coexpressing lymphoid markers: different biologic features between T-cell antigen positive and B-cell antigen positive AML. 848 20

Acute leukemias (ALs) with phenotypic and genotypic features of several hematopoietic lineages are difficult to classify and may represent the transformation of multipotent stem cells. We have studied immunological features of 200 cases of acute leukemia (109 acute myelogenous leukemia, AML, and 91 acute lymphoblastic leukemia, ALL, according to FAB criteria), including 17 (8.5%) classified as biphenotypic by a scoring system based on the number and specificity of unexpected lineage antigens and which gives more weight to cytoplasmic markers such as myeloperoxidase, CD3, and CD22, and less to other membrane markers. Sixty-eight AML and 42 ALL cases were also examined for rearrangements of the immunoglobulin (Ig) and T-cell receptor (TCR) beta, gamma, and delta genes, and these included 12 biphenotypic AL. The expression of myeloid antigens in ALL was seen in 25% of the cases. All B-lineage ALL had rearrangements and/or deletions of the Ig genes whereas TCR beta, gamma, and delta genes were rearranged in 21%, 52%, and 71%, respectively. TCR delta, gamma and/or beta were rearranged in T-ALL and four out of 13 cases had Ig gene rearrangement. Lymphoid-associated antigens were expressed in 40% of AML cases; those most frequent expressed were CD7 (17%), CD2 (15%), CD19 (10%), and CD10 (7.5%). Evidence of Ig and/or TCR gene rearrangements was detected in 12% of AML cases. There was no correlation between the isolated expression of terminal deoxynucleotidyl transferase (TdT), B, and T-cell antigens with Ig and TCR gene rearrangements. However, in cases of AML defined as biphenotypic because they expressed two or more lymphoid antigens there was a statistically significant correlation between gene rearrangements and lymphoid score (p < 0.001). Our findings support the concept of biphenotypic leukemia as a distinct entity in which there is frequent correspondence between phenotypic and genotypic changes.
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PMID:Lineage commitment in biphenotypic acute leukemia. 850 86

Correlation between the FAB classification and immunophenotype was studied in 169 consecutive adult patients with acute leukaemia (AL). The lineage of leukaemic cells could be determined in the majority of cases, whereas 3 patients (1.8%) remained unclassified. In 22 out of 71 patients (31%) with acute myeloid leukaemia (AML) FAB M1 and M2 types, and in 5 out of 16 patients (31%) with chronic myeloid leukaemia (CML) in myeloid blast crisis, leukaemic cells did not express myeloid lineage-related markers, indicating asynchronous expression of cell markers in a substantial proportion of patients. Flow cytometric two-colour immunofluorescence revealed mixed AL immunophenotype in 6 out of 169 patients (3.4%). This group included five CD2+AML (5% of AML tested) and one undifferentiated AL expressing CD10(CALLA), CDw65(VIM-2). The former group included FAB M1, M2, M3 and M4 forms of AML with a single cell population, and an AML M2 patient with both cytochemically and immunologically two separate populations of leukaemic cells. This further illustrates the heterogeneity of the target cell(s) for leukaemogenesis and the level of differentiation of AML cells. However, there was no difference in the treatment response and the remission duration between AML patients and patients with mixed phenotype AML.
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PMID:Correlation of morphological FAB classification and immunophenotyping: value in recognition of morphological, cytochemical and immunological characteristics of mixed leukaemias. 851 29

The clinical significance of the expression of lymphoid-associated antigens in leukemic cells was studied in 66 children with newly diagnosed acute myeloid leukemia (AML). Among 66 AML cases, 17% were CD7-positive, 15% were CD19-positive, 8% were CD2-positive, and 5% were CD10-positive. In 23 (35%) of the 66 AML cases, at least one lymphoid-associated antigen was expressed in the leukemic cells. When the clinical features and laboratory findings were compared at diagnosis between the 23 Ly+ and the 43 Ly- AML cases, no statistically significant difference was found. The expression of CD34 was significantly more frequent in Ly+ AML cases (91%) than in Ly- AML cases (31%). Chromosomal analysis revealed t(8;21) in 6 of the 21 Ly+ AML cases examined. No other specific chromosome aberration was noted. The 3-year event-free survival rates of Ly+ AML cases and Ly- AML cases were 34% +/- 12% and 26% +/- 8%, respectively. There was no statistically significant difference between the two groups. Further studies are required to determine the prognostic significance of lymphoid-associated antigen expression.
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PMID:Clinical significance of childhood acute myeloid leukemias expressing lymphoid-associated antigens. 851 31

We describe a patient with primary myelodysplastic syndrome (MDS) evolving into acute nonlymphocytic leukemia (ANLL) who had two cytogenetically unrelated abnormal clones. A 68-year-old man presented with refractory anemia with excess of blasts (RAEB) and developed overt ANLL. Two cytogenetically independent clones, one with 5q- and the other with 20q-, were observed when the patient developed ANLL. The clones carrying both 5q- and 20q- were not detected. Leukemic blast cells were positive for peroxidase, naphtol ASD chloroacetate esterase, CD13, CD33, CD34 and HLA-DR, but negative for alpha-naphthyl butyrate esterase, CD14, CD10, CD19, CD20, CD1, CD2, CD3, CD5 and CD7. Although there have been a few reports describing the presence of multiple cytogenetically unrelated clones in one patient with MDS, this is the first case report that the 5q- and 20q- anomalies are derived from independent clones.
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PMID:Two karyotypically unrelated clones with 5q- and 20q- in a primary myelodysplastic syndrome patient evolving into acute nonlymphocytic leukemia. 859 Jul 73

The clinical application of recombinant human G-CSF in patients with acute myeloid leukemia (AML) has been controversial because it stimulates the in vitro proliferation of leukemic cells. In order to explore the possibility of predicting in vivo leukemic proliferation after G-CSF administration to AML patients by using in vitro assays, we investigated the leukemic blasts of 30 AML patients, including 14 patients who received G-CSF for severe infection associated with neutropenia following chemotherapy (G-CSF group) and 16 patients who did not (control group). Of the 14 patients in the G-CSF group, 9 showed an increase of leukemic blasts in the peripheral blood during G-CSF administration, while 11 of the 16 control patients developed leukemic resurgence. In the G-CSF group, the frequency of leukemic resurgence among patients whose blasts showed dose-dependent proliferation after addition of G-CSF to cultures was similar to that among patients whose blasts did not. In addition, there were no significant differences between the G-CSF and control groups in [3H]thymidine incorporation by leukemic cells and leukemic colony formation after the addition of G-CSF to cultures. The G-CSF receptor affinity of leukemic blasts was significantly higher in the patients with leukemic resurgence (mean dissociation constant [Kd]: 55 pM in the G-CSF group and 63 pM in the control group) than in those without it (101 pM and 96 pM, respectively), and the number of G-CSF receptors per cell was significantly lower when leukemic resurgence occurred (200 in the G-CSF group and 260 in the control group) than when it did not (3400 and 3030, respectively). Immunophenotyping (for CD2, CD7, CD10, CD13, CD19, CD33, CD34, CD71, HLA-DR, glycophorin A and the G-CSF receptor) revealed no significant differences between blasts from the patients with and without leukemic resurgence in the G-CSF group. Thus, we conclude that the in vivo leukemic resurgence during G-CSF administration after chemotherapy for AML was not correlated with the in vitro responsiveness of leukemic blasts to this cytokine or with blast phenotyping data. Leukemic resurgence is likely to occur in patients whose leukemic blasts have fewer numbers of G-CSF receptors with a high affinity irrespective of whether patients receive G-CSF.
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PMID:Granulocyte colony-stimulating factor in acute myeloid leukemia. 859 Aug 66

We have analyzed the frequency and clinical significance of the MLL gene rearrangements in 42 cases of infant acute leukemias; including 37 cases of acute lymphoblastic leukemia (ALL) and five cases of acute myeloid leukemia (AML). MLL gene rearrangements were found in 27 of the 37 ALL cases (73 percent), and in all five AML cases. Cytogenetic studies showed 11q23 abnormalities in 24 of 27 ALL cases with MLL gene rearrangements. MLL gene rearrangements were significantly correlated with absence of CD10 expression and poor prognosis, but not with age under 6 months, hyperleukocytosis, myeloid-associated antigen expression, or CNS leukemia. The 3-year overall survival rate for ALL cases with MLL gene rearrangements was 5.3 +/- 5.2 percent, compared with 88.9 +/- 10.5 percent for cases with germline MLL (P=0.0001). Absence of CD10 expression was also associated with poor prognosis (9.9 +/- 6.6 percent vs 85.7 +/- 13.2 percent, P = 0.0003). Of the five AML cases, three have remained alive for 27 months to 67 months. These findings suggest that infant ALL with MLL gene rearrangement is strongly associated with poor prognosis. We consider that infant ALL should be treated on different chemotherapy protocols according to the presence or absence of MLL gene rearrangement.
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PMID:Frequency and clinical significance of the MLL gene rearrangements in infant acute leukemia. 870 35

Morphologic, immunologic, cytogenetic, and clinical features were studied in 9 cases of acute undifferentiated leukemia (AUL). These patients were unclassifiable by FAB criteria, they were CD34+ and did not express myeloid- or lymphoid-associated antigens (CD13, CD33, CD14, CD15, CD61, CD19, CD10, CD22, CD7, CD2, CD5, CD3). Clonal abnormalities were seen in 8 of 9 cases. Del(5q) as the sole anomaly was observed in 3 cases; +13 was the primary change in 3 cases, and isolated trisomy 12 was found in 1 patient. A complex karyotype with trisomy 12q, in association with del 17p and trisomy 21q was detected in 1 case. One patient with 5q- relapsed with refractory anemia with excess of blasts; the presence of dysgranulopoiesis and a few blasts with possible monocytoid morphology in the remaining 2 patients point to a "myeloid nature" of these leukemias. Analysis of cytologic features in our 3 patients with +13, in combination with previously reported cases, suggests the occurrence of immature stem cell involvement with limited differentiation potential, possibly more along the myeloid than the lymphoid lineage. The significance of trisomy 12q in this subset of leukemia remains elusive; some clues of minimal differentiation towards the myeloid lineage in our cases are provided by positivity for the CD117 (c-kit) antigen and by relapse with acute myeloid leukemia without maturation (M1) in one patient. We conclude that, with presently available diagnostic techniques, AUL is a rare subset of leukemia, in which cytogenetic changes are confined to a few chromosomes, with prevalent involvement of 5q and of chromosomes 13 and 12. Chromosome findings may be of value in clinical practice, especially in those cases with "myeloid-oriented" karyotype.
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PMID:Cytogenetic and clinicobiological features of acute leukemia with stem cell phenotype: study of nine cases. 895 68


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