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)

Over a two-year period, immunophenotypic patterns of 266 acute leukemia cases were analyzed using a panel of tests including TdT, SmIg and 9 surface antigens by the immunofluorescence stains for the assessment of the incidence and grade of phenotypic ambiguity (lineage infidelity) and the possible clinical significance of unusual immunophenotypes. Immunophenotypes were classified into four groups according to the degree of ectopic antigen expression. We classified as Group A (91.7%, 244 of 266 cases) those expressing conventional pattern without ectopic antigen. Group B (3.0%, 8 of 266 cases) was defined to have at least two lineage specific markers and single ectopic antigen. Such a "low grade deviation" did not prevent a definite immunodiagnosis. Group C (4.2%, 11 of 266 cases) revealed a promiscuous coexpression of markers related to different lineages, including two cases (0.8%, 2 cases) of biphenotypic leukemia. Group D (1.1%, 3 cases) included unclassifiable immunophenotypes with no antigen or HLA-DR only expression. Both patients with biphenotypic leukemia and one patient with unclassifiable immunophenotypes failed to respond to induction chemotherapy, suggesting a poor prognosis in these patients. The incidence of acute myelogenous leukemia (AML) cases with one or more ectopic surface antigens was 10 (8.1%) of the 124 AML cases. Ectopic antigen expression was seen in 5 (4%) of the 125 B-lineage acute lymphoblastic leukemia (ALL) cases and 3 (25%) of the 12 T-ALL cases. It is concluded that nearly 95% of cases of acute leukemia cases can be diagnosed accurately with immunophenotyping alone including patients with a mild degree of deviation from expected antigenic patterns.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute leukemias with unusual immunophenotypes. 129 44

We analyzed the rearrangement of T-cell receptor (TcR) delta chain gene in 196 cases of hematological malignancies. This rearranged band (s) was observed in 15% of the total cases investigated. All T-ALL patients and cell lines, except for P30/Okubo, had a new band (s) or deletion of J delta 1 gene locus, indicating the gamma delta T-cell type or the alpha beta T-cell type. In the other T-cell malignancies, the delta rearranged band (s) was recognized in 5% of T-cell lymphomas, 20% of AILD but not in ATL, Hodgkin's disease, T-CLL. Inappropriate delta rearrangement was frequently recognized in 63% of B-ALL and 50% of CML-BC but none or few (5% less) in B-CLL, B-lymphoma and AML. Southern blotting, using J delta 1 and V delta gene probes or Pst I enzyme digestion, indicated that the inappropriate delta rearranged band in B-ALL and CML-BC is V delta 2D or DD without a J delta locus. The rearranged band (s) involved J delta locus, was mostly recognized in 5/6 cases of CD7 (+) stem cell leukemia. Therefore, the TcR delta gene is useful in evaluating clonality for the most immature T-cell neoplasms, not showing rearrangement of the other TcR genes. Moreover, this delta gene may be a useful tool for distinguishing T-lineage from the other lineages, using the characteristic rearrangement pattern (V delta 2D as a inappropriate pattern, or (D) DJ and V (D) DJ as the T-lineage pattern (s)).
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PMID:[Analysis of T-cell receptor delta chain gene in hematological malignancies]. 132 69

Anti-CD34 is a monoclonal antibody that reacts with bone marrow progenitor cells and leukemic blasts, and is expressed on 30% to 50% of all acute leukemias. Detection of CD34 has previously been restricted to flow cytometric studies. To expand the utility of CD34, we immunostained 46 paraffin-embedded bone marrow specimens with acute leukemia; results were compared with flow cytometric studies. CD34 reactivity was also evaluated in nine chronic leukemia cases, 27 malignant lymphoma cases (Hodgkin's disease and non-Hodgkin's lymphoma), six normal bone marrow specimens, and three benign, hyperplastic lymph node specimens. All cases that were CD34 positive by flow cytometry (11 of 19 B-cell precursor acute lymphoblastic leukemia cases, one of six T-cell acute lymphoblastic leukemia cases, and seven of 21 acute myeloblastic leukemia cases) were also CD34 positive in paraffin sections. Both cell membrane and cytoplasmic staining was seen. The positivity percentage and fluorescence intensity by flow cytometry correlated with the estimated number of stained cells and the intensity of immunoperoxidase staining in 18 of 19 CD34-positive cases. The remaining bone marrow and lymph node cases studied were CD34 negative; prominent endothelial cell staining, however, was noted. This is the first report of anti-CD34 staining of acute leukemia in paraffin-embedded sections. In contrast to other monoclonal antibodies reactive in bone marrow paraffin sections with leukemia, anti-CD34 immunoperoxidase staining is limited to leukemic blasts and may provide useful diagnostic information when flow cytometric studies are not available.
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PMID:Anti-CD34 immunoperoxidase staining in paraffin sections of acute leukemia: comparison with flow cytometric immunophenotyping. 137 85

Fifteen cases of acute lymphoblastic leukemia (ALL) with translocations involving 9p and/or 12p are described. Four children, three males and one female, age range 1-8 yrs, had translocations involving 9p but not 12p. Of these, three had B-lineage ALL and one had biphenotypic T-ALL/acute myeloid leukemia. Six patients, three males and three females, age range 1-49 yrs, had translocations involving 12p but not 9p. Five had B-lineage ALL and one had T-ALL. One patient had dic(7;12)(p11;p11), confirming that this previously reported translocation is nonrandom in ALL. One patient had t(2;12)(q14;p13), and it is suggested that this may also be a new nonrandom abnormality. Five patients, four males and one female, age range 11-21 yrs, had common ALL and dic(9;12). The dic(9;12) appears to confer a better prognosis than do other translocations involving 9p or 12p.
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PMID:Translocations involving 9p and/or 12p in acute lymphoblastic leukemia. United Kingdom Cancer Cytogenetics Group (UKCCG). 138 80

Circulating immune complexes (ClC) were estimated in 78 patients of leukaemias and lymphomas by Clq deviation ELISA and PEG assay. In all leukaemias a significant elevation in ClC was seen at the time of first presentation. While in ALL a decrease occurred on therapy as partial or complete remission was achieved, no such fall was seen in AML or CML-BC when treated. ClC levels were much higher in non-Hodgkins lymphoma than in Hodgkins disease and showed a direct correlation with B symptoms and activity of the disease. The ClC levels were highest in null-ALL followed by those in common ALL and T-ALL. The mean duration of remission in patients of ALL without elevation in ClC was much longer than in those with ClC.
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PMID:Circulating immune complexes in leukaemias and lymphomas. 139 53

The clinical utility of the indirect immunofluorescence (IF) and the alkaline phosphatase-anti-alkaline phosphatase (APAAP) techniques was compared in 103 newly diagnosed acute leukaemia patients immunophenotyped using a panel of 19 monoclonal antibodies (MoAb). In spite of slight variations in the percentages of cells reacting with particular MoAbs when comparing the two methods we found no discrepancies in the final classification of each case. In ANLL (n = 73) the best correlation between the two methods was found for CDw65 which is a good screening marker, and for CD15 having a prognostic significance. In ALL (n = 30) the best correlation was observed for CD19 and CD10, both of great diagnostic importance. The following antigens present both in membrane and in cytoplasm displayed higher positivity with the APAAP than in IF HLA-Dr, CD71 and CD11b in ANLL, CD22 and HLA-Dr in nonT-ALL and CD3 in T-ALL. The important advantages of the APAAP technique are: 1) its use with routinely performed bone marrow or peripheral blood films, which can be stored before staining, 2) the possibility of correlating morphology with immunological characterization and documentation of the results.
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PMID:[Comparison of clinical usefulness of immunophenotyping of leukemia using the immunofluorescence and immunoenzyme APAAP methods]. 148 65

We studied 137 cases of acute leukaemia seen between December 1985 and November 1988, using traditional staining techniques together with cytochemistry and in cases of probable acute lymphoblastic leukaemia (Sudan Black negative) by immunophenotyping. Not all tests were carried out in every case (some cases of ALL could only be classified as T or non-T). Paediatric group (age less than or equal to 14 yrs): 75 cases--acute lymphoblastic leukaemia 52, acute myeloid leukaemia 18, acute undifferentiated leukaemia 5. Peak incidence in 5-9 year group. Male:Female ratio = 1.7:1. acute myeloid leukaemia was associated with chloromas in 2 cases (11 pc). Adult group: 62 cases--acute lymphoblastic leukaemia 23, acute myeloid leukaemia 36 and acute undifferentiated leukaemia 3. Peak incidence in 50-54 age group. Male:Female ratio = 1:1.2. Acute lymphoblastic leukaemia subtypes (all ages) T 16, Common 20, Null 12, 'non-T' 16, B cell 0, untyped 11. 69 pc were of L2 morphology. In T-ALL, 11 had thymomas and Male:Female ratio = 15:1. Male:Female ratio for 'non-T' = 1.5:1. Acute myeloid leukaemia subtypes (all ages) M1 3, M2 8, M3 14, M4 19, M5 8, M6 2, M7 1. Overall incidence of acute leukaemia appears increased at 0.91 per 100,000 per annum from previous studies in Zimbabwe. Common ALL (mean age = 13 years) is an emerging problem and now outnumbers T-ALL (mean age = 10 years). This may be related to a general improvement in living standards and health in Zimbabwe.
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PMID:A three-year prospective study of 137 cases of acute leukaemia in Zimbabwe. 151 27

Detection of minimal residual disease (MRD) can be useful for adaptation or stratification of treatment in acute leukemia patients and may finally result in individualization of treatment protocols. Although leukemic cells generally have immunophenotypes comparable to their normal counterparts, it is possible to use immunological marker analysis for the detection of MRD based on the assumption that the presence of positive cells outside their normal breeding sites and 'homing areas' is indicative of malignancy. This approach can be used for the detection of MRD in blood and bone marrow of patients with a terminal deoxynucleotidyl transferase (TdT) positive T-cell acute lymphoblastic leukemia (ALL) and patients with a TdT+ acute myeloid leukemia (AML) as well as in cerebrospinal fluid of patients with a TdT+ leukemia. In other types of acute leukemias, immunological marker analysis generally does not allow detection of low frequencies of malignant cells, but in a part of them the polymerase chain reaction (PCR) technique may be valuable. The PCR technique allows the amplification of tumor-specific DNA sequences or mRNA sequences (after reverse transcription into cDNA), if the flanking sequences are well-defined. This PCR-mediated amplification can detect specific sequences which are derived from only a few malignant cells between many normal cells. Well-defined chromosome translocations have been used as tumor-specific markers, such as t(9;22). An advantage of using specific chromosome aberrations as tumor-specific markers is their stability during the disease course. However, only 10-15% of ALL and 25-30% of AML have a specific chromosome translocation and in a large part of them the precise breakpoints are not (yet) known. Recent studies indicate that it is possible to detect MRD in acute leukemias by use of PCR-mediated amplification of the junctional regions of rearranged immunoglobulin (Ig) and T-cell receptor (TcR) genes, using variable (V) and joining (J) gene-specific oligonucleotides as primers. Major pitfalls of this application are the occurrence of multiple rearrangements at diagnosis (oligoclonality) and changes in rearrangement patterns at relapse (clonal evolution), which will lead to false negative results of this MRD-PCR technique. In conclusion, the technique of choice for the detection of MRD is dependent on the immunophenotype of the leukemia, the presence of a well-defined chromosome translocation and the presence of a rearranged Ig and/or TcR gene as well as the chance of immunophenotypic shifts and changes in Ig and TcR gene rearrangement patterns.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Detection of minimal residual disease in acute leukemia by immunological marker analysis and polymerase chain reaction. 154 36

Seven hundred and forty-four newly diagnosed patients with acute leukemias between 1978 and 1990 were classified on the basis of immunological phenotypes. The majority of the patients were enrolled in the Tokyo Children's Cancer Study Group (TCCSG) studies. The incidence of subclassification of acute leukemias in this study was as follows: 522 patients with ALL (70%), 139 patients with ANLL (18%), 29 patients with biphenotypic leukemia, 8 patients with Ph1-positive acute leukemia (Ph1-AL), and 45 patients with infant leukemia. ALLs were classified into common ALL (cALL, 77%), T-ALL (15%), B-ALL (4%), and unclassified ALL (3%). The incidence of ALL subtypes in this study reflected those of TCCSG. Biphenotypic leukemias were categorized into 4 groups as follows; 1) cALL with positive myelomonocytic antigen(s) (N = 11), 2) unclassified ALL with positive myelomonocytic antigen(s) (N = 5), 3) ANLL with positive B-lymphoid antigen(s) (N = 4), and 4) acute leukemia with positive T-lymphoid and myeloid antigen(s). Infant leukemias were classified into ALL type (N = 27) and ANLL type (N = 18). In this present study, clinical features and immunological phenotypes of the acute leukemias with a poor prognosis, i.e. biphenotypic leukemia, Ph1-AL, and infant leukemia are analyzed and discussed.
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PMID:Immunological classification of childhood acute lymphoblastic leukemia. 179 11

Leukemia karyotypes were analyzed in 792 children with acute lymphoblastic leukemia (ALL) and 217 patients with acute myelocytic leukemia (AML). These patients were registered and uniformly treated in German multicentre trials from 1984-01-01 to 1989-12-31. In distinct leukemia subgroups specific chromosome abnormalities were found: Numerical aberrations such as hyperdiploidy over 50 chromosomes in c-ALL or structural aberrations (translocations) such as t(8;14) in B-ALL, t(11;14) in T-ALL, t(4;11) in ppB-ALL, t(1;19) in pB-ALL, t(15;17) in AML-M3, t(8;21) in AML-M2. Prognostic significance of the leukemia karyotype probably can be changed by intensive cytotoxic chemotherapy. Unfavorable prognosis, however, still persists in t(9;22) and t(4;11); "favorable" prognosis can be seen in t(8;21) and t(15;17). Inherited or induced chromosome instability is discussed as a possible predisposing factor for the origin of chromosome aberrations.
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PMID:[Chromosome aberrations in acute leukemia in childhood: analysis of 1009 patients]. 183 89


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