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)

A 16 year-old boy was admitted to our hospital in April 1985, because of bilateral submandibular swellings. Hematological examination revealed Hb was 7.3 g/dl, WBC was 89,000/microliters (76% blast), and platelet was 154,000/microliters. His bone marrow was hypercellular and consisted with 91% blasts. Myeloperoxidase staining was positive for 38% of blasts. Auer rods were seen in some of blasts. Thus, the diagnosis was M1 according to FAB classification. Cytogenetic studies of 20 marrow cells were performed and all cells had 46, XY, -1, -7, 3q-, 7q-, 17q+, +2mar. Eighty five percent of blasts expressed HLA-DR and 43% of blasts expressed CD2 and CD13 simultaneously. Thus, this leukemia was considered as the hybrid type of acute mixed leukemia by surface marker analysis. DBMP-85 regimen, the chemotherapy for AML, was started after admission and complete remission (CR) was attained in June 1985. After 4 courses of post remission chemotherapy, he discharged in December 1985 and was followed at our outpatient clinic without chemotherapy. His disease was relapsed in June 1986, and the combination chemotherapy with mitoxantrone, etoposide and Ara-C was applied to him but failed to attain CR. Then, LVP protocol, the chemotherapy for ALL, was started and CR was achieved. The blasts at relapse had morphologically myeloid features, and expressed HLA-DR, CD2 and CD13 as well as at diagnosis. Cytogenetic studies at relapse showed some karyotype except gaining 12p- anomaly. Therefore, same blasts were considered to emerge at relapse. Our case suggests that LVP therapy may be effective for AML expressing myeloid and lymphoid surface markers.
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PMID:[DBMP-85 was effective at diagnosis and LVP was effective at relapse in a case of acute mixed leukemia]. 236 35

We have analysed the immunological characteristics of blasts from 89 acute lymphoblastic leukaemia (ALL) cases (62 adults and 27 children), by using a panel of antilymphoid and myeloid associated monoclonal antibodies (McAb) and the APAAP method, which detects membrane and cytoplasmic expression of antigens. The McAb CD19 was the marker most consistently expressed in B lineage ALL, being positive in 100% of cases, compared to CD24 and CD22 expressed in 82% and 79%, respectively. Similarly, for the T lymphoid lineage, the McAb CD3 was the most reliable and specific marker, being expressed in all T-ALL cases including those with an early thymic phenotype (CD7+, TdT+). Lymphoblasts from eight adults (12.9%) and three children (11.1%) expressed one to four myeloid associated antigens recognized by CD13, CD14, CD33 and anti-myeloperoxidase. There were no substantial clinical and morphological differences between the two ALL groups with or without myeloid associated markers. However, the presence of myeloid associated markers in adult ALL was associated with a significantly lower complete remission (CR) rate (P = 0.05) and with a shorter survival (P = 0.001); this variable was independent of advanced age and high WBC. It is concluded that immunophenotypic analysis in ALL should include myeloid markers for its probable prognostic implications.
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PMID:Clinical significance of the presence of myeloid associated antigens in acute lymphoblastic leukaemia. 237 6

During the diagnostic investigation of 750 acute leukemias, nine cases were morphologically, cytochemically, and phenotypically undifferentiated. In seven of these cases the blasts were class II+, CD34+ and TdT+, in one were class II+, TdT+, CD7+ while in the remaining leukemia blasts expressed class II only. Cytoplasmic and membrane CD22, CD3, CD13, and Ig as well as membrane CD19, CD10, CD37, CD2, CD33, CD14, glycophorin C, and CD61 were absent. The further characterization of these rare leukemias yielded the following results. The TCR-beta, -gamma and -delta genes were in germline configuration in seven cases studied while IgH genes were rearranged on both alleles in two cases and germline in the other five. By ultrastructural analysis peroxidase activity was detected on unfixed cells in a minority of blasts from four of seven cases. In two of the peroxidase-positive cases a small proportion of blasts also reacted with an anti-myeloperoxidase monoclonal antibody. In one of the peroxidase-negative cases, 7% of blasts were labeled by the antibody, suggesting the presence of peroxidase in its proenzyme form. Importantly, the two cases with Ig gene rearrangements did not have cytochemically or immunologically detectable peroxidase. Three of the nine patients were treated as ALL while six received AML chemotherapy. In five patients complete remission was achieved while the other four died from infections during remission induction. Four patients are still in remission 7, 12, 24, and 30 months after diagnosis while one patient relapsed after 12 months. In conclusion, we have characterized the genotypic and ultrastructural features of subtype of acute leukemia in which blasts expressed immaturity markers and lacked lineage associated antigens. In contrast to previously reported "unclassifiable" cases, the leukemias were phenotypically homogeneous and showed a good response to chemotherapy.
Leukemia 1990 Sep
PMID:Phenotypic, genotypic, cytochemical, and ultrastructural characterization of acute undifferentiated leukemia. 239 82

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.
Leukemia 1989 Mar
PMID:The reliability of cytoplasmic CD3 and CD22 antigen expression in the immunodiagnosis of acute leukemia: a study of 500 cases. 246 63

A 12-year old boy was admitted to Saitama Children's Medical Center because of fever and epistaxis. He had leukocytosis (WBC 40,800/microliters, blast 75%), anemia, thrombocytopenia and high levels of serum LDH, lysozyme, Vitamin B12, and plasma histamine. Bone marrow aspiration revealed hypercellular marrow with 31.2% blasts, 15.2% eosinophils, and 14.2% basophils. Blasts had Auer rods and were positive for peroxidase and negative for alpha-naphthyl butyrate esterase and PAS stainings. Ia, CD13 (My7), and CD19 (B4) antigens were expressed on his leukemic cells. Chromosomal study showed 46, XY, t(7;8) (q35;q22), del(9) (q13q22). Southern blot analysis using immunoglobulin constant region (C) probes revealed germline patterns of C mu, C kappa, C lambda, and breakpoint cluster region. A diagnosis of acute myelomonocytic leukemia (AMMoL, M4) was made. He attained a complete remission with daunorubicin and cytarabine, and 6 months later he received bone marrow transplantation from HLA-identical sister. This case had the common breakpoint 8q22 with ANLL with t(8;21) (q22;q22), and was unique AMMoL with proliferation of eosinophils and basophils in bone marrow.
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PMID:[Acute myelomonocytic leukemia (M4) with CD19 antigen expression, eosinophilia and basophilia in bone marrow]. 247 65

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 megakaryoblastic leukemia (FABM7) is an unusual but well recognized form of acute myelogenous leukemia in which the bone marrow blast cells are phenotypically recognized by the demonstration of cytoplasmic platelet peroxidase or surface staining for the IIb/IIIa platelet-specific glycoprotein. Herein, the authors report a case of acute megakaryoblastic leukemia that satisfies the accepted French-American-British criteria and in which the blast cells also exhibit evidence of myeloid differentiation, including surface MY7 (CD13) by flow cytometry and immunocytochemical positivity for myeloperoxidase. These findings suggest that megakaryoblasts may be closely related to myelomonoblasts, that they have the potential to partially differentiate along multiple phenotypic lines, and that aberrant phenotypes can occur that do not correspond to known stages of normal maturation. The authors illustrate the difficulty in classification of these aberrant phenotypes by standard cytochemical and morphologic criteria.
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PMID:Myeloperoxidase-positive acute megakaryoblastic leukemia. 254 7

A 26-year-old male was admitted to our hospital because of fever and leukocytosis. On admission, a white blood cell count was 28,300/microliters with 46.5% blast cells and 16.0% atypical monocytoid cells, a hemoglobin level 13.7 g/dl, and a platelet count 15.0 X 10(4)/microliters. Bone marrow contained 58.8% of peroxidase-negative blast cells. He was diagnosed as acute lymphoblastic leukemia (ALL L2) according to the FAB classification. Chromosome analysis revealed the marrow cells to contain 45, XY, -7, t(9; 22) (q34; q11). On surface marker analysis, the leukemic cells were positive for both lymphoid (CD10) and myeloid markers (CD13). Two color flow-cytometric analysis showed two distinct populations with CD10 and CD1 3, respectively. Rearrangements of both immunoglobulin heavy chain and T cell receptor beta-chain were observed. The "breakpoint cluster region" on chromosome 22 was not rearranged. On the basis of these findings, we thought this case being acute mixed leukemia. He was refractory to AdVP therapy and BHAC-DMP therapy. He is now under treatment with A-Triple-V therapy.
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PMID:[Philadelphia-positive acute mixed leukemia with monosomy 7]. 255 34

Some of the many cell-surface antigens defined by the CD (cluster differentiation) nomenclature have lately emerged as proteins with well-characterised enzymic activities. One important example is CD10 or CALLA (common acute lymphoblastic leukaemia antigen), which is identical to endopeptidase-24.11, an enzyme with an important role in the hydrolysis of biologically active peptides. CD13 and CD26 are also surface peptidases. These enzymes, which have a wide distribution on the surfaces of various cell types, may have specific roles in the control of growth and differentiation in both haemopoietic and epithelial cell systems.
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PMID:Cell-surface peptidases as modulators of growth and differentiation. 257 Oct 20

A case of chronic lymphocytic leukemia (CLL) treated with chlorambucil, followed by the development of an acute monoblastic leukemia, is described. Cytofluorometric quantitative immunophenotype was determined during the blastic phase. Whereas small lymphocytes displayed a CD19+; CD24+; CD37+; CD5+ phenotype, the blastic population exhibited, besides CD13, CD14 and CD15 positivity, which is usually noted in such a monoblastic leukemia, definite CD9, CD10, CD22, CD24, CD37, CD5 and CD4 staining. Such results argue against a complete independence between the two clones, although their similarity could not be demonstrated.
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PMID:Acute monocytic leukemia with B cell markers expression following B chronic lymphocytic leukemia. 258 3


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