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)

Current views about the origin of acute lymphoid leukemia (ALL) emphasize the importance of maturation arrest at a precursor cell level. Recently, the CD22 antigen has been identified in the cytoplasm of normal bone marrow-borne immature B lineage cells, while the CD3 antigen (epsilon chain) has been detected within normal immature thymic blasts. In the first part our study performed on 100 cases of known acute leukemias, the expression of such cytoplasmic molecules, referred to as cCD22 and cCD3, was analyzed together with their appearance in the leukemic cells' membrane (mCD22 and mCD3). The presence of cCD22 in B-lineage ALL and that of cCD3 in T-ALL has indeed fully confirmed the diagnosis reached by other markers, and mCD22 and mCD3 were expressed on only a few cases of B- and T-lineage ALL, also revealing a degree of developmental asynchrony within leukemic blasts. In the subsequent analysis both cCD22 and cCD3 have been included in a standard panel of diagnostic reagents applied on 500 consecutive cases of acute leukemia. Here the aim was to analyze both the diagnostic precision of individual markers and the heterogeneity of various leukemic types in terms of the expression of membrane and intracellular antigens and their cytochemical features (Sudan Black B and esterases). It has been found that cCD22 and cCD3 are exquisitely specific for B-precursor ALL (TdT+, CD19+) and T-ALL (TdT+, CD7+), respectively, while both markers are absent in acute myeloblastic leukemia (AML) and acute myelomonocytic and monocytic leukemia (AMML/AMoL). These observations contrast the findings which demonstrate that 31% of cases among nonlymphoid acute leukemia (including AML and AMML) express CD7 and/or TdT. The study of myeloid antigens detected by CD13, CD33, and CD14 is also informative and complementary, both in diagnosing and subdividing the AML and AMML/AMoL groups. The peculiar main observation of this study is that only with the combined use of these markers in a microplate assay for membrane antigens, followed by double staining for intracellular antigens such as terminal deoxynucleotidyl transferase, cCD3, cCD22, c mu heavy chain, and T cell receptor beta, it is possible to safely establish the lineage affiliation and subgrouping of virtually all acute leukemias. Among these cases are those with aberrant combinations of markers, including 14% of B-lineage ALL (cCD22+,CD19+,TdT+) and a single case T-ALL (cCD3+,CD7+,TdT+), which exhibit CD13 and/or CD33 antigens, cases with mixtures of ALL and AML blasts, and 1.2% of acute leukemias which lack lineage affiliation and can be regarded as acute undifferentiated leukemia.
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PMID:The reliability of cytoplasmic CD3 and CD22 antigen expression in the immunodiagnosis of acute leukemia: a study of 500 cases. 246 63

Seventeen patients with acute myeloid leukaemia (AML) whose blasts co-expressed the T-cell associated CD7 antibody were identified among 160 consecutive AML cases. Fourteen had FAB defined AML according to morphocytochemical criteria, whereas three patients were classified as 'MO' on the basis of immunophenotype. The incidence of CD7 positively was particularly significant in the less differentiated subtypes M0 and M1 compared with other FAB groups (P less than 0.001). In all cases the myeloid determinants CD13 and/or CD33 were associated with CD7 expression. Other B-lymphoid (CD10, CD19) or T-lymphoid (CD2, surface and cytoplasmic CD3) markers were analysed and found to be negative. Five out of 15 cases examined were TdT+. Clonal rearrangements of the immunoglobulin heavy chain (IgH) and/or T-cell receptor (TcR) beta chain genes were identified in only three out of 13 cases. Among these, one out of five co-expressing TdT showed IgH rearrangement when analysed at the DNA level. Clinical features at presentation and response to induction therapy did not allow us to consider CD7+ AML patients as a distinct subgroup with prognostic significance. Our data indicate that CD7 expression is a common finding in immature AML, being generally found in the absence of other T-cell features. Rather than suggesting the occurrence of 'mixed leukaemia', such cases confirm a broader spectrum of CD7 reactivity and its possible identification of a particular subset of myeloid progenitors.
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PMID:CD7 positive acute myeloid leukaemia: a subtype associated with cell immaturity. 248 63

Acute leukemia was diagnosed in 62 adults and children over a recent 13-month period. Using light microscopy, cytochemical profiles, surface markers, and cytogenetics, 25 cases were classified as acute myeloid leukemia (AML) and 32 as acute lymphoblastic leukemia (ALL). The remaining 5 cases of de novo acute leukemia were unclassifiable. The routine cytochemical battery used on these 62 cases included: myeloperoxidase, sudan black B, nonspecific esterase, and periodic acid-Schiff (PAS). Flow markers utilized were: T3, T4, T5, T8, T10, T11, B1, B4, kappa, lambda, Ia, CALLA, Mo1, Mo2, My4, My7, My8, and My9. TdT was performed by immunoperoxidase and ELISA methods. The five unclassified cases were cytochemically negative and expressed no B- or T-cell-specific antigens, or TdT positivity. The morphologic differential diagnosis was between FAB L-2 and M-1. Karyotypic abnormalities involving chromosomes 3 and 7 were suggestive of myeloid origin in 2 of 4 patients studied. Flow cytometry demonstrated My7 on greater than 50% of blasts from two cases. Myeloperoxidase ultracytochemistry showed reaction product in small primary granules of blasts from all 5 cases. Positive cells contained only 1-2 granules/cell profile. The number of positive cells per case was in the range 10-20%. We conclude from this study that ultracytochemistry is very useful in providing definitive diagnosis and accurate subclassification of some AML FAB M-1 cases, particularly when light microscopic cytochemistry, cytogenetics, and flow cytometric markers are noncontributory. We propose to designate these acute "unclassified" leukemias as AML FAB M-1 "microgranular" type.
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PMID:Acute myeloid leukemia, FAB M-1 microgranular variant: a multiparameter study. 254 66

The immunophenotype of 135 previously untreated patients with FAB defined acute myeloid leukaemia (AML) was studied at diagnosis. The panel of reagents included monoclonal antibodies (MoAb) recognising myeloid-associated determinants (CD11, CD13, CD14, CD33 and others) as well as MoAb directed towards lymphoid antigens (CD7, CD10, CD19) and TdT. The results indicate that CD13 and/or CD33 are consistently expressed in AML and only rarely in ALL blasts (131/135 + ve cases, versus 4/130 in ALL). Lymphoid antigen expression was rarely detected when CD10 and CD19 were investigated in AML (0.9% and 2% + ve cases, respectively), whereas significant positivities were found for TdT and CD7 (20% and 10% respectively). Concerning FAB subtypes, two new MoAb (LAM3 and LAM7) proved very useful in the specific recognition of AML with monocytic features. The phenotype CD13+ and/or CD33+, CD9+, HLA-DR- was found to be almost exclusive for M3 AML. The response to induction chemotherapy was analysed in CD7+ and in TdT+ patients. In the latter group a statistically significant lower response rate was found with respect to TdT-ve-AML patients.
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PMID:Immunophenotyping of acute myeloid leukaemia: relevance of analysing different lineage-associated markers. 272 Jan 73

The levels of TdT, AdA, 5'-N, 20 alpha-SDH and TK1 were analyzed in different FAB subgroups of AML. AdA, 5'-N, 20 alpha-SDH and TK1 showed large variations both within and between the different subgroups. It therefore seems unlikely that measurements of these enzymes will be able to aid morphological subclassification of AML. Neither could analysis of these enzymes give prognostic information. TdT was detectable in 46% of AML but the levels were only 1/10-1/100 of those found in ALL. The enzyme was detected in leukaemic granulocytopoietic cells while leukaemic cells of monocytic origin were negative in all but 1 case. In addition, increased TdT activity was positively correlated to the length of survival.
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PMID:Enzyme markers in acute myeloid leukaemia. 300 21

Anti-CD3 (T3) Ab reacting with different proportions of thymocytes (anti-CD3a: UCHT1, anti-CD3b: T10B9, and anti-CD3c: OKT3) were tested for cytoplasmic (cCD3) and membrane (mCD3) expression in the bone marrow, thymus, and blood in man and selected primates. The expression of cCD3a and cCD3c in the perinuclear and Golgi area of large, BrdU-incorporating, strongly TdT+ thymic blasts probably represents one of the earliest signs of T cell commitment, because these blast cells are CD1-, CD4-, CD8-, and mCD3-. The cCD3+, TdT+ cells are normally restricted to the thymus and are absent among the TdT+ cells of bone marrow. The anti-CD3b Ab used, T10B9, co-caps and co-modulates with the other anti-CD3 Ab and is a T cell-specific reagent at a membrane level but does not bind to perinuclear cCD3. Instead, this reagent cross-reacts with a filamentous cytoplasmic network in non-T cells in man and in primates S. oedipus and M. rhesus despite their T cell negativity for mCD3. The characteristics of all T-ALL cases studied: cCD3+, CD7+ along with nuclear TdT+ suggest lineage fidelity to early thymic blasts. As a marked contrast, cCD3 is absent in common ALL and in AML, including cases that concomitantly express CD7 and myeloid antigens. Thus, the cCD3, TdT combination provides a very sensitive assay for residual T-ALL blasts outside the normal thymus.
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PMID:The cytoplasmic expression of CD3 antigens in normal and malignant cells of the T lymphoid lineage. 309 52

A case of acute leukaemia with t(4;11) chromosomal abnormality in a 28-year-old woman is reported. At diagnosis, two blast cell populations were seen: 60% of the cells were small cells with lymphoid morphology, 40% were large cells with monocytic morphology. Cytochemical examination was consistent with acute myeloid leukaemia (peroxidase-positive in 10% of the cells), but surface markers were those of common acute lymphoblastic leukaemia (CALLA, B4, TdT-positive, but My7-, My9- and OKM1-negative). Five days after diagnosis, although the only treatment had been platelet transfusions, there was a change in morphological and immunological phenotype: 40% of the cells were lymphoid and 60% monocytic. Lymphoid markers were expressed in only 20-40% of cells, and myeloid markers appeared on up to 60% of cells. We conclude that t(4;11) leukaemia could originate in an undifferentiated progenitor cell, which can undergo further differentiation into lymphoblasts or monoblasts, and that we were able to observe this in vivo differentiation in our patient.
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PMID:Variations in morphological and immunological blast cell phenotype in a case of acute leukaemia with t(4;11) translocation. 310 60

One hundred ninety-two patients with previously untreated AML had TdT studies performed on their presenting BM aspirate specimens. Thirty-seven patients (19%) had greater than 5% TdT-positive (TdT+) blasts in their BM, as determined by an indirect immunofluorescence technique. CR rates were similar in both groups of patients (20/37 vs. 97/155, p = not significant) as were remission durations and median survivals. In the subset of patients younger than 60 years, patients with TdT+ blasts had an increased median survival (110 vs. 54 weeks, p = 0.1) compared with those having TdT- blasts. Six of 37 patients with TdT+ findings had t(8;21) translocations compared to 5 of 155 with TdT- findings (16% vs. 3%, p less than 0.01). Patients with more than 50% BM blast cells showing TdT positivity at diagnosis tended to be younger than those with TdT- (mean age 30.5 years and 50.3 years, p = 0.04). The presence of TdT+ blast cells in the initial marrow in patients with AML may be associated with specific cytogenetic abnormalities and may identify subsets of patients who have improved prognoses.
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PMID:Cytogenetic association and prognostic significance of bone marrow blast cell terminal transferase in patients with acute myeloblastic leukemia. 317 42

The method to fix single cells in suspension and its application for the detection of TdT-positive cells by flow cytometry are described. In comparison to formalin-methanol fixation, formalin-acetone fixation resulted more formation of aggregated cells which caused non-specific staining. In our assay system 80% cells in human thymus were TdT-positive. Levels of TdT in normal human peripheral blood was 0.5 +/- 0.6% (means +/- 1 S.D., n = 50). A total of 104 patients with leukemia/lymphoma was examined for TdT. TdT-positive cells were detected in ALL (87.5% cases), AML (57.1% cases), CML-BC (58.3% cases) and ML (17.6% cases). Mean channel of fluorescence intensity of the TdT-staining in AML was significantly reduced in comparison with that in ALL. When antigen density of TdT was very low, fluorescence microscopy gave false negative results and flow cytometry could detect this dim fluorescence.
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PMID:Enumeration of terminal deoxynucleotidyl transferase positive cells in leukemia/lymphoma by flow cytometry. 329 65

Early studies of terminal transferase (TdT) expression in acute leukemia indicated that this enzyme is only found in acute leukemia of lymphoblastic type (ALL). More recently, however, several reports have suggested that TdT-positive blast cells may be found in a substantial number of cases of acute myeloid leukemia (AML). In this study, a sensitive immunoalkaline phosphatase procedure (the APAAP technic) has been used to stain normal and neoplastic blood and bone marrow samples for TdT with the use of both polyclonal and monoclonal anti-TdT antibodies. As expected, most cases of ALL studied (63 of 65) were TdT-positive. In addition, however, blast cells in 22 out of 59 (37%) cases of AML were stained by anti-TdT antibodies. Both nuclear and cytoplasmic localization were seen in each type of acute leukemia. These findings, together with previous immunocytochemical and biochemical studies, suggest that a substantial number of cases of AML express TdT (usually in a minority of blast cells) and that the frequency with which these cases are detected is directly related to the sensitivity of the staining technic used.
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PMID:Immunoalkaline phosphatase labeling of terminal transferase in hematologic samples. 330 Feb 65


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