Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.11 (CD10)
 9,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the multicentric trial LALA87 was to test the efficacy of different postremission therapies in adults (15 to 60 year olds) with acute lymphoblastic leukemia (ALL). An immunologic subclassification based on surface marker expression was proposed. Among the 562 tested patients, 511 were assigned either to the B lineage (361 cases, 63%) or to the T lineage (150 cases, 26%). T-ALL were significantly associated with male sex, age less than 35 years, mediastinal mass, central nervous system involvement, high white blood cell count, and low anemia. In a univariate and multivariate analysis, T-cell leukemia had a more favorable outcome than B-cell leukemia with respective median disease-free survivals (DFSs) of 28 and 14 months (P < .005). However, the type of postremission therapy modifies the value of the immunophenotype prognostic factor. In the chemotherapy arm, T-ALL patients (26 patients) had a more favorable outcome than B-ALL patients (57 patients) (P < .003). In the autologous bone marrow transplantation (ABMT) arm, the apparent better outcome of T-ALL patients (35 T/50 B) did not reach statistical significance (P = .2) and there was no difference in the allogeneic bone marrow transplantation (alloBMT) arm (37 T/71 B: P = .9). In the B-cell-lineage leukemias, subclassification by stages and myeloid antigen coexpression (10%) were not associated with different prognosis. CD10+ T-ALL (31 patients) were associated with a better DFS compared with the CD10- T-ALL (73 patients) with respective median DFS, not reached and 18.5 months (P = .04).
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PMID:Immunophenotype of adult acute lymphoblastic leukemia, clinical parameters, and outcome: an analysis of a prospective trial including 562 tested patients (LALA87). French Group on Therapy for Adult Acute Lymphoblastic Leukemia. 806 49

The expression of the Ig-linked mb-1 polypeptide was analyzed by immunocytochemistry (alkaline phosphatase anti-alkaline phosphatase technique) using a specific monoclonal antibody in 165 cases of acute leukemia, with 88 being lymphoblastic (ALL) and 77 myeloid (AML). The purpose of the study was to investigate the specificity of this reagent for B-lineage cases and its reactivity on leukemias that coexpress myeloid and B-cell antigens (biphenotypic). The majority (89%) of 72 B-cell precursor ALL patients were positive. Of these, mb-1 was expressed in all 9 patients with early-B-ALL (CD10-, c mu-), in all 11 patients with pre-B-ALL (c mu+) and in the single case of B-ALL (smIgM+). Forty-three of 51 patients with common-ALL (CD10+, c mu+) were also positive. All 16 T-lineage ALL patients and 72 (93.5%) of the AML patients examined were mb-1 negative. Four of the 5 mb-1-positive AML patients were considered biphenotypic and expressed other B-cell antigens such as CD10, CD19, and/or cCD22 and all showed rearrangement of the Ig heavy chain genes. Within the AML cases, mb-1 and cCD22 were more useful than other B-cell antigens in detecting biphenotypic cases, and mb-1 showed the highest correlation with the clonal rearrangement of Ig heavy chain genes. These results indicate that mb-1 is a sensitive and specific reagent for B-lineage blasts that will aid in the classification of B-cell precursor ALL and in the identification of biphenotypic leukemia presenting as AML.
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PMID:mb-1: a new marker for B-lineage lymphoblastic leukemia. 833 49

Immunophenotype and age have prognostic value in childhood acute lymphoblastic leukemia (ALL) but how this operates is not understood. In 84 children with ALL at initial diagnosis we studied the correlation between these factors and the in vitro resistance to eight drugs, determined with the 3-(4,5-dimethylthiazol-2-yl-2, 5-diphenyl tetrazolium bromide (MTT) assay. B-lineage ALL samples were classified into four differentiation stages: the CD10- proB ALL; cALL; preB ALL with cytoplasmic mu positive ALL cells; and B-ALL with surface immunoglobulin-positive (Ig+) cells. cALL and preB ALL cases have the best prognosis; proB and T-ALL cases show a worse prognosis and B-ALL the poorest prognosis. Patients aged < 18 months and > 10 years have a poor prognosis compared to patients in the intermediate age group. Our results show that cALL and preB ALL cells were the most drug-sensitive cells compared to the other phenotypes. No differences were found between cALL and preB ALL cases with the exception that preB cells were more sensitive to mustine and mafosfamide (Maf). Compared to cALL and preB ALL cases, T-ALL cases were significantly more resistant to prednisolone (Pred), daunorubicin (DNR), L-asparaginase (L-Asp), cytosine arabinoside (AraC), and Maf; proB ALL cases were more resistant to Pred, DNR, L-Asp, and 6-thioguanine. The three B-ALL cases were resistant to vincristine and DNR. Two out of three B-ALL were resistant to Pred. Compared to cells from patients aged 18 months to 10 years, cells from children < 18 months were more resistant to Pred and DNR; cells from children > 10 years were more resistant to Pred. We conclude that cellular drug-resistance patterns might at least partly explain the prognostic value of immunophenotype and age in childhood ALL.
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PMID:Cellular drug resistance profiles that might explain the prognostic value of immunophenotype and age in childhood acute lymphoblastic leukemia. 844 45

Peripheral blood, bone marrow and/or lymph nodes of 77 patients with T- and B-ALLs/lymphomas were characterized for their surface membrane marker profiles using flow cytometry and fluorescence microscopy. Purine metabolism enzyme activities were compared with membrane immunophenotypes. T and B-ALLs/lymphomas subtypes were defined by the expression of surface membrane antigens detected by the monoclonal antibodies. Based on immunophenotyping we found the following characteristic marker profiles: in T-ALL-CD7, CD2, CD1, CD5, CD3, CD4, CD8, CD38, CD71; in T-NHL-CD7,CD2,CD3,CD4,CD5,CD6; in pre-B ALL-CD10, CD19, CD24, HLA-DR, CD34, in B-ALL-CD19, CD20, CD24, HLA-DR, SmIg with kappa or lamda light chains; in B-ALL-weak SmIg, kappa or lambda, CD19, CD20, CD24, CD5, HLA-DR; in B-NHL-CD19, CD20, CD22, CD24, CD5, more intensive SmIg, kappa or lambda. The cells of leukemic cases tended to have more immature phenotypes than those of lymphoma cases. Analysis of purine metabolism enzyme activities showed that there was a correlation between the values of adenosine deaminase (ADA) and purine nucleoside (PNP) and various types of T- and B-ALLs/lymphomas. ADA levels in B-NHL and B-CLL were lower than those in normal cells, while ADA level in T-ALL, T-NHL, pre-B-ALL and B-ALL was higher (the average 185,92,73,63 pkat. 10(-6)cells, respectively). ADA activity was significantly different between lymphocytes of control group and T-ALL(p<0.01), between T-ALL and T-NHL(p<0.05), between T-NHL and B-NHL(p<0.05) and between T-ALL and B-NHL(p<0.05). PNP activities were lower to those in normal cells. ADA/PNP ratio increased mostly in T-ALL, less in T-NHL, pre-B-ALL and B-ALL (10.8 and 5.3 and 2.2, and 2.0 respectively). ADA/PNP ratio was significantly different between T-ALL and pre-B-ALL(p<0.05) and between T-ALL and B-NHL(p<0.05).
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PMID:A comparison of some leucocyte differentiation markers and the adenosine deaminase and purine nucleoside phosphorylase values in B and T cell leukemias and lymphomas. 859 72

Because activated T cells were previously shown to induce proliferation of human normal B-cell precursors (BCP) via the CD40 pathway, we investigated the effects of T cells on leukemic blasts isolated from patients with B-lineage acute lymphoblastic leukemia (BCP-ALL). An anti-CD3 activated human CD4+ T-cell clone was found to induce significant call proliferation in four of nine BCP-ALL samples analyzed. In one of these cases, the T-cell effect was clearly dependent on interaction between CD40 and its ligand. Accordingly, a more thorough analysis was performed on this particular leukemia (case 461, adult early pre-B-ALL, mBCR+, Philadelphia+, i(9q)+). Thus, autologous CD4+ T cells isolated from the patient were also able to induce CD40-dependent proliferation of the leukemic blasts. Analysis of the phenotype after coculture showed that, among the CD19+ cells, a proportion gradually lost expression of CD10 and CD34, whereas some cells acquired CD23. In addition, and in contrast with normal BCP, activated T cells promoted maturation of a subset of the case 461 leukemic cells into surface IgM+ cells. The leukemic origin of the cycling and the maturing cells was assessed by the presence of i(9q), a chromosomal abnormality associated with this leukemia and evidenced by fluorescence in situ hybridization. Taken together, these results show that leukemic BCP can be activated via CD40 but that not all cases display detectable stimulation in response to T cells despite their expression of CD40. In addition, the present data suggest that CD4+ T cells could potentially play a role in the physiology of BCP-ALL.
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PMID:Demonstration of functional CD40 in B-lineage acute lymphoblastic leukemia cells in response to T-cell CD40 ligand. 865 29

Bone marrow and peripheral blood from children with acute lymphoblastic leukemia was analyzed by flow cytometry to assess leukemic cell differentiation and to characterize the profile of cell surface marker expression on rare CD34+ cell populations. The goal of this study was to determine if patterns of cell surface antigens could be identified on CD34+ subpopulations which may allow distinction between normal and leukemic stem cells. Expression of the progenitor cell antigen CD34 on leukemic blasts was very heterogeneous and varied between 0.5 and 100% in 20 patients analyzed in this study. In cALL and pre-B-ALL, a variable percentage of the leukemic cells coexpressed CD20 in addition to CD10. Only in one case, differentiation characteristic for normal B cell development with coordinated downregulation of CD10 with increasing expression of CD20 was observed. By analysing 5 x 10(6)-1 x 10(6) cells, a CD34+ cell population could be identified in 8 out of 8 patients which did not express CD19 and comprised less than 0.1% of all bone marrow or peripheral blood cells. Within this population, there was differentiation from primitive CD34-CD38- to more mature CD34+CD38+ cells. In 4 of these patients, an additional CD34+ population with low expression of CD19 (CD34+CD19lo) was detected. The lack of CD45 expression on the leukemic cells of 2 patients was used as a marker for the leukemic cell clone. In both patients, the CD34+CD19- cells did express CD45 while CD34+CD19lo/+ cells were CD45 negative. This suggests that the CD34+CD19lo cells were part of the leukemic clone and that the CD34+CD38-CD19- cells may represent residual normal primitive hematopoietic cells. In conclusion, flow cytometry allowed identification of primitive CD34+ cell populations in children with ALL, which can now be functionally characterized by transplantation onto immune-deficient mice.
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PMID:[Flow cytometric characterization of maturation processes and primitive stem cell population in pre-B-cell ALL in childhood]. 892 82

Over a time period of five years leukemic blast samples from 141 consecutive patients with adult ALL were referred to our laboratory, for molecular evaluation of chromosome abnormalities. The t(9;22), t(4;11) and t(1;19) which are most commonly found in adult ALL with a B-precursor phenotype were molecularly analyzed by similar RT-PCR based protocols. BCR-ABL transcripts generated by the t(9;22) translocation were demonstrated in 36 patients (25%) and were restricted to the 109 patients with B precursor ALL (33% of this group). Of 83 patients showing a, common phenotype (CD10+), 34 were BCR-ABL positive (41%) whereas only 2 out of 26 with Null ALL (HLADr+, CD19+, CD10) were positive. Interestingly, the percent of BCR-ABL positive CD1O+ ALL increases significantly with age being 20% in patients less than 30 years old and more than 50% in older patients. None of the T-ALL (24 patients) and B-ALL (8 patients) were positive. The majority of cases (67%) showed the p190 gene subtype. The cytogenetic diagnosis of Philadelphia chromosome was always confirmed by the molecular analysis and this approach allowed for the detection of the presence of the BCR-ABL rearrangement in 26 patients when a negative result or no metaphases were obtained. The complete remission rate was similar among BCR-ABL positive and negative patients but a shorter remission duration was observed in those showing molecular evidence of t(9;22) and this finding was significantly evident in CD1O+ ALL patients. By means of comparison, in most of the same adult ALL patients, we analyzed the yet unrecognized prevalence of the t(4;11) and t(1;19) translocations by the molecular analysis of their chromosomal breakpoints. Rearrangements of the ALL-1 gene on 11q23 band and ALL- l1AF.4 fusion transcripts specific for the t(4;11) were demonstrated in 7 out of the 21 Null ALL investigated, with no additional positive cases found among the other ALL subgroups. Overall the clinical behavior of t(4; 11) positive patients was dismal with a very short CR duration. Chimeric E2A-PBX1 transcripts generated by the t(1;19) were found in only two of the 87 B-precursor ALL analyzed. The presented results provide further evidence for the utility of RT-PCR based methods for the molecular diagnosis of chromosome translocations in ALL. The identification of such abnormalities can significantly contribute to the identification of more appropriate therapeutic options for standard and high risk ALL patients
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PMID:Molecular diagnosis and clinical relevance of t(9;22), t(4;11) and t(1 ;19) chromosome abnormalities in a consecutive group of 141 adult patients with acute lymphoblastic leukemia. 917 11

A total of 119 children (1990-95) with acute lymphoblastic leukemia (ALL) B-lineage either CD10+ or CD10- were registered into a single non-randomized chemotherapy protocol. Only untreated patients with standard risk were included in the study. Their ages ranged from 1.8-10 years with a mean of 5.1 years. There were 82 (68%) children with early pre B-All, 35 (29%) with pre B-ALL and 2(1.6%) with transitional pre B-ALL (p < 0.00001). The patients were divided according to CD10 reactivity, either + (94 children) or -(25 patients). The event-free survival (EFS) at 60 months for the CD10+ children was of 78% (alive 73/94), while for the CD10- was 71% (alive 18/25) (p = 0.6) and 74% for both groups. The factors that influenced favorably the survival in the CD10+ group were the age between 3 to 5.99 years (p < 0.00001), sex (either male or female), leukocyte count between 10-24.9 x 10(9)/l (p < 0.00001), LDH under 300 U/I (p < 0.00001) and L1 bone marrow cytomorphology (p < 0.00001). In the CD10- patients, the EFS was favorably influenced by the female sex (p = 0.04), leukocyte count under 10 x 10(9)/l (p = 0.05) and LDH < 300 U/l (p = 0.02). CNS infiltration was documented in 4.2% (5/119). Mortality secondary to chemotherapy was seen in 7%. In conclusion, this is the first large series in Mexican children with B-lineage ALL published. Because of the relatively small number of patients in each group (pre B and transitional pre B), all the patients in the current series were treated alike. When the 119 patients were divided only on the basis of CD10 reactivity, the EFS for both groups (CD10+ and-) was similar; therefore, the reactivity to CD10 has no prognostic value in this type of ALL.
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PMID:B-lineage acute lymphoblastic leukemia of childhood. An institutional experience. 920 15

CD66c is a surface (and intracellular) molecule bound to the membrane by a glycosyl-phosphatidylinositol anchor. While its expression on peripheral granulocytes is well recognized, less is known about its distribution in early steps of normal and neoplastic hematopoiesis. We analyzed by flow cytometry cell surface expression of CD66c on bone marrow cells from 4 healthy subjects and on bone marrow or peripheral blood cells from 127 patients with newly diagnosed hematologic malignancies: 70 de novo acute myeloid leukemias (AML), 6 refractory anemias with excess of blasts in transformation, 3 myeloid and 3 lymphoid blastic phases of chronic myelogenous leukemia, 33 B-lineage and 6 T-lineage acute lymphoblastic leukemias (B- and T-ALL), and 3 B-cell and 3 T-cell non-Hodgkin's lymphomas in the leukemic phase. We found that in normal bone marrow CD66c expression was myeloid restricted, reaching its highest level on promyelocytes. As for de novo AML, slight expression of CD66c was found on 6/25 (24%) AML-M4 and only occasionally in other subgroups. In 9 out of 10 cases of acute promyelocytic leukemia, CD66c was totally absent, but antigen expression was easily detectable following in vitro exposure to all-trans retinoic acid. Among lymphoid malignancies, CD10+ early-B-ALL consistently expressed the molecule (20/23 cases, or 87%) whereas both CD10- early-B ALL and SmIg+ B-ALL completely lacked it. Finally, dual staining with CD66c and CD10 proved to be a suitable tool for distinguishing even low percentages of residual leukemic cells (CD10+/CD66c+) from normal regenerating early-B cells (CD10+/CD66c ) in CD10+ early-B-ALL induced into remission.
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PMID:CD66c antigen expression is myeloid restricted in normal bone marrow but is a common feature of CD10+ early-B-cell malignancies. 971 68

Long-term follow-up of the rate of CD10, CD19 and CD34 antigens expression compared with the percentage of lymphocytes and blastic cells in 196 bone marrow specimens of 91 children with early B-cell acute lymphoblastic leukemia has been performed. It was shown that during a five year period there were no significant differences concerning the percentage of CD markers and the percentage of lymphocytes and blastic cells except those in the 4th year of clinical and immunological follow-up--when increase of lymphocytes and CD19 marker percentage have been observed. Consensus, i.e. more than 20% CD markers positivity associated with more than 5% blasts (positive consensus) or less than 20% CD markers positivity combined with less than 5% blasts (negative consensus) was ascertained in 92.8% of cases. Disagreement, i.e. the rate of CD markers over 20% combined with less than 5% blasts was found in 14 (7.2%) patients. This finding present in the initial phase of the disease could be considered as a sign of not complete remission, in contrast to the finding in children who completed chemotherapy and were in long-term hematological remission, in which the increase of CD markers could be considered as a sign of increased regeneration activity of bone marrow after chemotherapy induced medullary aplasia. Anyway, the increase of CD10, CD19 and CD34 antigens in bone marrow samples over 20% should be evaluated with caution. In these cases, mainly in children with long-term hematologic remission the examination should be repeatedly performed and/or more sensitive methods for detection of minimal residual disease should be applied. In control group of 20 children without leukemia the rate of CD markers in the bone marrow was always under 20%.
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PMID:Expression of CD10, CD19 and CD34 markers in bone marrow samples of children with precursor B-cell acute lymphoblastic leukemia in clinical and hematological remission. 989 Jun 66


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