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

Cytogenetic patterns in correlation with cytologic, biomolecular and clinical findings were studied in 45 adult patients with AML expressing at least one of the following lymphoid associated markers (LM): CD2, CD7, CD10, CD19, CD22, TdT. Four cytogenetic groups were recognized: group I, including 8 patients with 11q23 rearrangements; group II including 5 patients with the Ph chromosome; group III, with 19 patients and aberrations of the "myeloid type" including 4 cases with aberrations of chromosome 13, 3 cases with 1q and 7q anomalies, 2 cases with trisomy 11q; group IV, including 13 patients with normal karyotype. Patients showing extensive lineage infidelity were encountered more frequently in cytogenetic groups I and II than in groups III and IV. Two of 4 cases with aberrations of chromosome 13 showed two or more lymphoid features either at immunophenotyping or at biomolecular analysis of the configuration of lg and TCR genes. Patients with 11q23 rearrangements and with the Ph chromosome were generally young, presented with high WBC count and had low complete remission rate. Survival in Ph chromosome positive patients was uniformly short. We conclude that, although there is no cytogenetic anomaly specific for AML with LM, chromosome findings may be clinically relevant in AML with LM. A morphologic, immunologic and cytogenetic classification of AML with LM may constitute a working basis for future studies aimed at a better definition of clinicopathological features and optimal treatment strategy for these leukemias.
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PMID:Clinical review on features and cytogenetic patterns in adult acute myeloid leukemia with lymphoid markers. 834 65

Results of immunophenotypic examinations of peripheral blood and/or bone marrow (BM), involved in low-grade B-cell non-Hodgkin's lymphomas, were compared with the results of cytomorphological and histopathological examinations in 133 adult patients. 69 cases of chronic B-lymphocytic leukaemia (B-CLL), 16 centrocytic (CC) lymphomas, 14 centroblastic-centrocytic (CB/CC) lymphomas, 15 immunocytomas (IC), 10 cases of hairy cell leukaemia (HCL), four prolymphocytic leukaemias (PLL), two B-CLL in transformation, one splenic lymphoma with villous lymphocytes (SLVL), one hairy cell leukaemia variant (HCL-V), and one lymphocytic lymphoma (LC) were classified according to the Kiel and/or FAB classification. Leukaemic disease was found in 105 cases. The following markers were used for immunocytology (APAAP technique) of blood and/or BM smears: CD19, CD5, CD10, CD11c, CD14, CD21, CD22, CD23, CD25, CD38 and TdT. All cases tested showed CD19, but no TdT expression. Every case of HCL had a distinct phenotype with expression of CD11c, CD22 and CD25 and the lack of CD5 and CD23 antigens. In all other NHL cases a very heterogenous expression of CD-antigens with no significant correlations to the cytomorphological subtypes was found. The expression of CD5 is a frequent but inconstant finding in lymphoproliferative diseases other than B-CLL, so 50% of CB/CC, 75% of CC and 80% of IC were CD5 positive. Our results indicate that, with the exception of HCL, the diagnostic relevance of immunophenotyping for the classification of cytomorphologically and histopathologically defined subtypes in blood and/or BM is of very limited value.
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PMID:Immunophenotyping of low-grade B-cell lymphoma in blood and bone marrow: poor correlation between immunophenotype and cytological/histological classification. 825 6

During a period of 9 years, we performed immunological marker analysis in 164 children with acute lymphoblastic leukemia. In four children the diagnosis acute leukemia could not be established by cytomorphological analysis of bone marrow and peripheral blood samples at initial presentation. In two of these four children a hypoplastic bone marrow was found, whereas the bone marrow of the other two children was normocellular. Using double immunological marker analysis, we detected high frequencies of CD10+, TdT+ cells in bone marrow (range: 18-53%) as well as peripheral blood (range: 0.04-19.5%). In control bone marrow and peripheral blood samples from healthy children, the frequency of CD10+, TdT+ cells does not exceed 10% and 0.03%, respectively. Based on the immunological data, a common acute lymphoblastic leukemia (ALL) was suspected. In addition, chromosome analysis revealed a high hyperdiploid (> 50 chromosomes) karyotype in three patients and t(9;22) in one patient. At 18 to 68 days after initial presentation, an ALL was diagnosed according to cytomorphological criteria in all four patients. At that time the percentage of CD10+, TdT+ cells in bone marrow and peripheral blood had increased significantly. One patient could be monitored frequently from initial presentation onwards. First a decline in the percentage of CD10+, TdT+ cells was found, although treatment consisted only of red blood cell transfusion and antibiotics. Subsequently the percentage of CD10+, TdT+ cells gradually increased until the morphological ALL diagnosis. These results illustrate that CD10, TdT double immunological marker analysis is a useful tool for early diagnosis of smoldering ALL in patients with a suspicious bone marrow, even when the bone marrow is hypoplastic.
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PMID:Early diagnosis of smoldering acute lymphoblastic leukemia using immunological marker analysis. 846 31

The immunophenotype of 304 adult lymphoblastic leukemias (> 18 years) diagnosed on the basis of the FAB criteria was determined at the time of diagnosis using a panel of monoclonal antibodies. The series comprised cases diagnosed and immunophenotyped in 43 Italian centers (GIMEMA Cooperative Group) between April 1988 and June 1991. The immunophenotypic characterization consisted of two consecutive steps. The initial screening was based on the reactivity for TdT, HLA-Dr, CD7, CD10, CD13, CD19, CD24, CD33 and CD41. According to the results obtained, the second level of investigation assessed the positivity for intra cytoplasmic (Cy) Ig, CD1a, CD2, CD3, CD4, CD5, CD8 and CD20. Based on the hierarchical expression of the different B- and T-cell related antigens, each case was assigned to a given differentiation stage. B-lineage ALL were classified in five subgroups (B0-B4) and T-lineage ALL in four subgroups (T0-T3). Cases in which the blasts were lymphoid according to the FAB criteria, but expressed myeloid antigens in association with B- and T-lymphoid markers were defined as hybrid leukemias. As expected, CD10+ cases (B2-B3) were the most frequent within the B-lineage ALL (83.2% of cases). CyIg+ (B3) accounted for about 20% of CD10+ ALL. Twenty eight cases (13.4%) were at a pre-cALL stage (B0-B1) and of these, 8 (3.8% of the total series) were positive only for TdT and HLA-Dr (B0). Intermediate and mature thymic phenotypes (T2-T3) were predominant within the T-ALL (67.2%) groups. Five cases, were positive only for TdT and CD7 (CD5+), and classified as T0. 9.2% of cases fulfilled the definition of hybrid leukemia, largely in view of the co-expression of B-lymphoid and myeloid markers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunophenotype of acute lymphoblastic leukemia cells: the experience of the Italian Cooperative Group (Gimema). 847 81

We report a detailed analysis of a B cell defect affecting a patient girl born from first cousin parents, characterized by a severe non-X-linked agammaglobulinemia with a total absence of CD19- cells in the periphery. In the bone marrow, CD19 expression was also highly impaired, resulting in the absence of both B and preB compartments. By contrast, CD34+CD10+, CD34psiL+, and some CD19+CD10+ mostly CD34+ early proB cells were present, although diminished. Semiquantitative RT-PCR analysis performed on mononuclear bone marrow cells indicated that lambda-like, VpreB, Rag-1, Rag-2, and TdT transcripts expressed during proB cell stages were found at normal levels whereas E2A, CD10, Syk, Pax-5, CD19, Igalpha, Igbeta, VH-Cmu, and Vkappa-Ckappa transcripts characteristic of later stages were severely depressed. This phenotype resembles that of Pax-5 knock-out mice, but since the coding sequence of the patient Pax-5 cDNA was shown to be normal, the defect might rather result from an altered regulation of this gene. All these data indicate that the patient suffers from a new genetic defect that results in an arrest of differentiation within the proB cell compartment, i.e., earlier than X-linked agammaglobulinemia, before the onset of Ig gene rearrangements.
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PMID:A human non-XLA immunodeficiency disease characterized by blockage of B cell development at an early proB cell stage. 883 98

We describe a case of bilineal leukemia in a 5-year old boy with a rare immunophenotype and the novel translocation t(9;17)(p11;q11) as the sole chromosomal abnormality. Two immunologically distinct blast cell subsets expressed T-markers (CD2, CD5, CD7) and common ALL markers (TdT, CD19, CD22, CD10), respectively. Both cell populations were CD34 negative. The patient, who presented with CNS leukemia, responded promptly to standard chemotherapy for lymphoblastic leukemia and remains in complete remission 20 months from diagnosis. Other translocations between chromosomes 9 and 17 have been infrequently reported in a variety of leukemias but as yet their biologic significance is unknown. The clinical course of this case suggests that t(9;17)(p11;q11) may not have an adverse influence on the disease outcome. However, the role of t(9;17) in the pathogenesis of this unusual lymphoid phenotype remains unresolved.
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PMID:Bilineal acute leukemia of B and T lineage with a novel translocation t(9;17)(p11;q11). 913 Jun 26

We report a detailed comparison of B cell defects in two patients, one XLA and one non-XLA. Both had severe agammaglobulinemia with a total absence of CD19+ cells in the periphery. In the non-XLA case, CD19 expression was also highly impaired in the bone marrow, resulting in the absence of both B and preB compartments. Early proB cells were present since CD34+CD10+ and some CD19+CD10+ mostly CD34+ were identified, although diminished. By contrast, in the XLA patient the CD34+CD19+ proB cells were increased whereas the CD34-CD19+ preB cell population was low. Semi-quantitative RT-PCR analysis performed on mononuclear bone marrow cells from the non-XLA patient indicated that lambda-like, VpreB, Rag-1, Rag-2 and TdT transcripts expressed during proB cell stages were found at normal levels whereas E2A, CD10, Syk, Pax-5, CD19, Ig alpha, Ig beta, VH-C mu and V kappa-C kappa transcripts characteristic of later stages were severely depressed. By contrast in the XLA patient most of these transcripts were observed in normal amounts. The phenotype of the non-XLA patient resembles that of Pax-5 or Ig beta knock-out mice, but since the coding sequence of both cDNAs were shown to be normal, the blockage might rather result from an altered regulation of one of these genes or from defect of other genes. All these data indicate that the non-XLA patient suffers from a new genetic defect that results in an arrest of differentiation within the proB cell compartment, before the onset of Ig gene rearrangements. From all agammaglobulinemias reported so far, including XLA cases and those resulting from C mu gene defects, the non-XLA patient exhibits the earliest blockage in the B cell differentiation pathway.
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PMID:A non-XLA primary deficiency causes the earliest known defect of B cell differentiation in humans: a comparison with an XLA case. 923 32

A unique case with diffuse mixed malignant lymphoma was investigated for gene rearrangement on the level of T-cell receptor (TCR), heavy chain immunoglobulin (Ig), and both light chains. Cell phenotype was examined with immunofluorescence techniques using antibodies against surface immunoglobulins (SIg) and the kappa and lambda light chains. Monoclonal antibodies were used against CD3, CD4, CD5, CD8, CD10, CD19, CD22, HLA-DR, and TdT. Gene rearrangement analysis for monoclonality determination was carried out with restricted DNA (EcoR I and Hind III) hybridized with one of the following 32P-labelled probes: T-cell receptor (TCR beta), immunoglobulin heavy chain (JH), k light chain, and lambda light chain. Phenotyping of the cell population from the excised lymph node (LN) revealed the presence of 66% B-cells and 35% T-cells. Most of the B cells (94%) expressed mu heavy chain only. Expression of both light chains was negligible (k = 7% and lambda = 2%). Gene rearrangement, which indicates monoclonality, was positive on the level of TCR, Ig heavy chain, and both light chains. The data obtained suggests a neoplastic transforming event in lymphoid stem cells, which preceded the subsequent differentiation process into either B or T lymphoma.
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PMID:Lymphoma with multi gene rearrangement on the level of immunoglobulin heavy chain, light chains, and T-cell receptor beta chain. 972 88

This study prospectively analysed the relationships between immunophenotypic and cytogenetic features of blast cells in 432 acute non-lymphoblastic leukemias (ANLL) at presentation. An abnormal karyotype was detected in 232 cases (54%). These abnormalities were related to immunophenotypic markers as detected using a consensual panel of monoclonal antibodies allowing lineage assignment and investigation of myeloid marker expression on blast cells. In univariate analysis, CD9, CD10, CD15, CD34 and TdT expression appeared significantly associated with chromosomal anomalies. Multivariate analysis identified CD34 and CD9 expression as independently predictive of the presence of at least one cytogenetic abnormality (P < 10(-4) and P < 0.03, respectively). Significant associations between immunophenotypic and karyotypic features were observed both within individual FAB subgroups and independently from morphological criteria. Specific features were seen in five ANLL entities: M0 or M1/B lineage antigen positivity/t(9;22) or del(11)(q23); M2/CD13-/t(8;21); M4/CD13+, CD34+, CD36+/inv(16); M4 or M5/lack of B lineage antigen/del(11)(q23) or t(9;11). More practically, and although the relationships demonstrated only represent a fraction of homogeneous immunophenotypic subgroups, identification of such immunophenotypic features should prompt careful karyotypic examination, eventually using molecular biology analysis on non-growing cells.
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PMID:Immunophenotypic patterns and cytogenetic anomalies in acute non-lymphoblastic leukemia subtypes: a prospective study of 432 patients. 943 18

We hypothesize that early lymphoid commitment from primitive hematopoietic marrow progenitors is governed by signals from the marrow microenvironment leading to sequential induction of lineage-specific genes. Using expression of lymphoid genes as markers of differentiation, we characterize a highly purified population (>99.8% by double sorting) of primary human CD34+Lin-DR- progenitors. This population was then used to evaluate the effects of supplemental cytokines (interleukin-2 [IL-2], IL-3, IL-7, c-kit ligand), FLT-3 ligand (FL), and stroma-derived factors on lymphoid differentiation in vitro. CD3, RAG-1, Ikaros, CD10, and TdT transcripts were detected in the starting CD34+Lin-DR- population. By contrast, CD3gamma, CD3delta, CD3zeta, and RAG-2 transcripts were not present in any samples tested. The presence of supplemental cytokines alone at culture initiation permitted stimulation of the expression of CD3zeta, but not of CD3gamma or CD3delta. However, when FL and stroma-derived factors were added to cytokines, CD3 gene expression was induced in all samples. The predominant CD3 transcripts induced by optimal culture conditions were alternatively spliced isoforms lacking transmembrane sequences (CD3delta and CD3gamma) and portions of the intracellular and extracellular domains (CD3gamma). The combination of cytokines, FL, and stromal factors also provided a potent stimulus for RAG-2 gene expression. These findings show that FL in combination with stroma-derived factors provide important signals to promote early events required for lymphoid differentiation.
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PMID:FLT-3 ligand and marrow stroma-derived factors promote CD3gamma, CD3delta, CD3zeta, and RAG-2 gene expression in primary human CD34+LIN-DR- marrow progenitors. 947 32


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