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)

From 583 cases of acute lymphoblastic leukemia (ALL) and 181 cases of acute myeloid leukemia (AML) in childhood, seven patients were identified to have t(11;19) (q23;p13) by sequential cytogenetic analyses. The t(11;19) was associated with B-precursor ALL at diagnosis in three patients and at relapse in one patient. All four tested patients with B-precursor failed to express the CD10 antigen when the t(11;19) was detected, and one of three patients tested expressed myeloid-associated markers. In three other patients the translocation was detected either at lineage conversion from ALL to M5 AML (n = 2) or from AML to CD10- B-precursor ALL (n = 1). Leukemic blasts of four patients had an entirely different karyotype at the time of lineage conversion or loss of CD10 expression, suggesting an induction of a second neoplasm. Thus the t(11;19) can be found in de novo or secondary acute leukemia with lymphoid (CD10-) or myeloid (monoblastic) phenotype. Further investigation of the gene(s) involved in the 11q23 chromosomal region and the breakpoints in the 19p13 region is needed to understand the leukemogenesis of this apparently heterogeneous group of disorders.
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PMID:Childhood acute leukemia with t(11;19) (q23;p13). 177 55

The early stages of normal human B-cell differentiation were studied by flow cytometry and cell sorting based on expression of CD10 (CALLA) and CD19 antigens in fetal liver. Both CD10+ CD19+ and CD10+ CD19- precursor populations proliferated in vitro to form B-cell precursor colonies under stimulation from low molecular weight B-cell growth factor (L-BCGF) or recombinant interleukin 3 but did not respond to high molecular weight B-cell growth factor (H-BCGF). The colonies derived from the CD10+ CD19- fraction showed induction of CD19 expression in 10-50% of growing cells, suggesting that CD10 expression precedes CD19 expression in B-cell ontogeny. This hypothesis was corroborated by less-differentiated marker profiles of the progeny of CD10+ CD19- B-cell precursors as compared to CD10+ CD19+ B-cell precursors in BCGF-stimulated cultures and by higher percentages of CD10+CD19- versus CD10-CD19+ B-cell precursors. CD19 crosslinking on normal fetal liver or bone marrow B-cell precursors was associated with an increase in cytoplasmic calcium concentration, but was inhibitory for colony formation. Leukemic B-cell precursors from acute lymphoblastic leukemias (ALLs) differed from normal B-cell precursors in their in vitro proliferative responses, since (i) they responded not only to L-BCGF and rIL-3 but also to H-BCGF and (ii) their proliferation was stimulated rather than inhibited by CD19 crosslinking. A clonogenic leukemic counterpart for the CD10+CD19- normal B-cell precursor population does not exist among malignant cells from B-cell precursor ALL patients, suggesting that the CD19 receptor may be involved in leukemogenesis of human B-cell precursor ALL.
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PMID:Immunobiologic differences between normal and leukemic human B-cell precursors. 246 Aug 71

Although the origin of acute leukemia with the 4;11 translocation has been shown to be an early myeloid progenitor cell or a stem cell with the potential for differentiation into both lymphoid and myeloid lineage, few precise studies on acute leukemia with the 11;19 translocation have thus far been reported. This study focused on the clinical, morphologic, ultrastructural, and immunologic characteristics as well as the DNA in three cases of acute leukemia with the 11;19 translocation. All three patients were infants and showed hyperleukocytosis. The morphologic feature was French-American-British (FAB)-L2 in two patients, in one of which a few monocytoid blasts were also seen by electron microscopy. Cells from the third patient underwent morphologic changes from FAB-L2 at the time of diagnosis to M5b at relapse. Immunologic marker studies revealed that the blast cells from all three patients expressed Ia and B4, but none expressed B1, CALLA(J5), T antigens, or SIg. Cells from one patient simultaneously expressed myeloid antigen (MCS-II) both at diagnosis and relapse. Cells from two patients expressed myeloid antigen after being cultured for a short time in vitro. An analysis of immunoglobulin genes and T-cell receptor genes revealed rearrangements of the heavy chain genes and germ line configurations of the kappa and lambda light chain genes, and of the T-cell receptor beta chain genes. These findings suggest that acute leukemia with the 11;19 translocation has mixed lineage characteristics as a result of leukemogenesis in a stem cell with the potential for both lymphoid and myeloid, especially monocytic, differentiation.
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PMID:Immunoglobulin heavy chain gene rearrangements and mixed lineage characteristics in acute leukemias with the 11;19 translocation. 312 49

Clinical and laboratory features of seven patients with acute leukemia associated with the (4;11) chromosome translocation are presented. Leukemic blasts of these patients showed lymphoid morphology in 6 (although 1 was treated for monoblastic leukemia 3 years earlier) and monocytoid morphology in 1, were positive for TdT and HD 37 (CD 19) in 6 patients, whereas weak expression of CALLA was seen in only 1 patient and T-lineage-associated antigens in none. Leukemic blasts from four patients showed the simultaneous expression of B-lymphoid and myeloid antigens, suggesting leukemogenesis in a very early multipotent progenitor cell. In 2 patients an isochromosome of the long arm of No. 7 chromosome was found in the leukemic karyotypes in addition to t (4; 11) (q 21; q 23); in one instance present at diagnosis, in the other one occurring at relapse. In one other patient leukemia karyotype also demonstrated trisomy 8. Leukemic cells of three patients were investigated by molecular genetics and demonstrated immunoglobulin gene rearrangements for the Ig heavy chain sequences but not for the light chain constant regions and T cell receptor sequences. All patients were treated by intensive chemotherapy. Four of the 7 patients are in continuous complete remission. The longest event-free survival time (over 2 1/2 years) was seen in one patient who had also DOWN-syndrome. Including these 7 patients a clinical analysis of 71 patients with t (4; 11) acute leukemia was made, emphasizing the following characteristics at diagnosis: female sex (62%), age under 2 years (49%), leukocyte count over 100 X 10(9)/1 (61%), splenomegaly (80%), CNS-disease (11%). Survival of over 2 years was reported in less than 15% of the patients. It remains to be seen if risk-adapted treatment can alter the course of this early B-precursor acute leukemia with hitherto very bad prognosis.
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PMID:Acute leukemia with chromosome translocation (4;11): 7 new patients and analysis of 71 cases. 349 35

This report describes the clinical and laboratory features of seven cases of acute leukemia associated with the 4;11 chromosomal translocation. All seven children had acute lymphoblastic leukemia by standard morphologic and cytochemical criteria. Leukemic blasts from six of seven patients were terminal deoxynucleotidyl transferase-positive. Immunologic phenotyping suggested the leukemias were of B cell origin; blasts from five patients expressed HLA-DR and p24 (CD-9 antibody), blasts from three patients expressed B4 (CD-19), and blasts from two patients expressed the common acute lymphoblastic leukemia antigen (CD-10). One patient's leukemic blasts contained cytoplasmic immunoglobulin. Analysis of DNA from four of five patients demonstrated additional evidence of B cell differentiation with heavy-chain immunoglobulin gene rearrangement. When DNA from the four patients with heavy-chain immunoglobulin gene rearrangement was analyzed, one patient's DNA demonstrated light-chain immunoglobulin gene rearrangement. However, flow cytometric analysis of blasts from three patients showed the simultaneous expression of the lymphoid-associated antigen B4 (CD-19) and the myeloid-associated antigen My-1 (X-Hapten). Electron microscopic examination of blasts from one patient that expressed both lymphoid- and myeloid-associated antigens demonstrated ultrastructural characteristics of both lineages. These findings suggest that acute leukemia with the t(4;11) abnormality has mixed lineage characteristics as a result of leukemogenesis in a multipotential progenitor cell or aberrant gene expression later in differentiation. Furthermore, serial analysis of karyotype, immunophenotype, and heavy-chain immunoglobulin genes revealed changes in these biologic markers over time, suggesting continued chromosome rearrangement and gene modulation after the leukemogenic event in cells with the t(4;11).
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PMID:Clinical and laboratory characteristics of acute leukemia with the 4;11 translocation. 394 43

A human pro-B cell line, named JKB-1, was established from the bone marrow of a 16-year-old girl with acute lymphoblastic leukemia (ALL) in relapse. The origin of the JKB-1 cell line was indicated by its chromosomal and immunologic similarity to the patient's fresh leukemic cells. This cell line has been growing for more than 14 months in suspension culture medium and had a doubling time of about 24 hours. JKB-1 expressed terminal deoxynucleotide transferase (TdT) and early antigens (HLA-DR, CD19, CD24) of B cells, with heavy chain gene rearrangement. However, it did not express late antigens (CD10, CD20, CD21, CD22, CD23) of B cells, light chain gene rearrangement, and cytoplasmic mu-chain. These results suggested that JKB-1 is at the stage of "pro-B" cell or early B-cell precursors. This cell line was induced to differentiate after 7 days of co-incubation with irradiated bone marrow stromal cells because of the expression of pre-B cell antigens (CD10, CD20), cytoplasmic mu-chain, light chain gene rearrangement, and disappearance of TdT, JKB-1 cells adhered to a preestablished bone marrow stromal cell layer with string-like processes under scanning electron microscope. When JKB-1 cells were separated from the stromal layer by a cyclopore membrane with 0.45 micron pore size, they did not differentiate. Bone marrow stromal cell conditioned medium could not induce differentiation either. Thus it was suspected that direct contact between JKB-1 cells and stromal cells was required for differentiation. In methylcellulose semisolid medium, the colony size and number of JKB-1 cells were increased by stem cell factor (SCF), or interleukin (IL)-3, or IL-7, but they were decreased by IL-6. Moreover, SCF synergized with IL-3 or IL-7 to stimulate the proliferation of JKB-1 cells. Because there are very few reproducible models for examining early stages of human B-cell differentiation, the JKB-1 cell line would be useful for studying the relationship between human B-cell differentiation and bone marrow microenvironment, as well as leukemogenesis.
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PMID:Establishment of a human pro-B cell line (JKB-1) and its differentiation of preestablished bone marrow stromal cell layer. 817 77

Alteration of the TAL1 locus is the most common nonrandom genetic defect in childhood T-cell acute lymphoblastic leukemia (T-ALL). To determine if rearrangements of the TAL1 proto-oncogene confer a distinct leukemic phenotype, we studied leukemic peripheral blood or bone marrow samples from 182 children with newly diagnosed T-ALL enrolled on Pediatric Oncology Group treatment protocols. Forty-eight (26%) of the samples had a local rearrangement of the TAL1 locus. Demographic and clinical features were compared for patient subgroups with and without TAL1 rearrangements. The only clinical correlates that were significantly associated with TAL1 gene rearrangements were higher white blood cell count (P = .017) and higher hemoglobin (P = .007) at diagnosis. Immunophenotypically, samples with altered TAL1 were more likely to be CD2+ (P = .001) and lack CD10 (cALLa) expression (P = .007) than those without the rearrangement. There was a trend toward improved event-free survival (EFS) in patients with TAL1 rearrangements (4-year EFS was 44% +/- 7% for patients without the rearrangements v 59% +/- 11% for those with rearrangements), but the difference was not significant (P = .34). The role of TAL1 in leukemogenesis has yet to be clearly defined, and the prognostic significance of TAL1 gene rearrangements in T-ALL deserves further study.
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PMID:Clinical features and outcome of T-cell acute lymphoblastic leukemia in childhood with respect to alterations at the TAL1 locus: a Pediatric Oncology Group study. 847 69

A new B-cell line (VL51) with cytoplasmic villi was established from a female patient with splenic lymphoma with circulating villous lymphocytes (SLVL). The patient exhibited a clinical picture characteristic of SLVL, including massive enlargement of the spleen. Tartrate-resistant acid phosphatase (TRAP)-negative villous lymphocytes were seen in the peripheral blood, bone marrow (BM) and both red and white pulps of the spleen. Monoclonality of the VL51 cell line was confirmed by clonal genotype abnormalities in the immunoglobulin heavy chain (IgH) gene and the T-cell receptor beta (TCR beta) gene. Evidence for commitment of phenotype of the VL51 cell line to the B lineage was also shown by the immunophenotype, including expression of CD10, CD19, CD20 and surface immunoglobins. The VL51 cells were positive for Epstein-Barr virus nuclear antigen (EBNA). The VL51 cell line is the first SLVL cell line to be established, and it is expected to be useful in clarifying the leukemogenesis of SLVL.
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PMID:Establishment and characterization of a villous lymphoma cell line from splenic B-cell lymphoma. 855 98

To investigate the clinical implications of germline C mu transcription, the splice region between the 3' end of the enhancer and the first exon of immunoglobulin germline mu; was analyzed by RT-PCR in 63 samples from 59 patients with leukemia. Immunophenotypes of 33 samples from patients with acute leukemia were analyzed using a panel of these monoclonal antibodies: anti-immature/stem cell (HLA-DR, CD34); anti-mature myeloid (CD33, CD15); anti-T lymphoid (CD2, CD3, CD5, CD7, CD8), and anti-B lymphoid (CD10, CD19, CD20). Of the 63 samples, 33 (52%) contained germline C mu transcripts: 2/2 patients with chronic lymphocytic leukemia; 17/26 (65.4%) patients with acute myeloblastic leukemia; all 4 patients with chronic myelogenous leukemia in blast crisis and 1 in accelerated phase; 9/12 patients with acute lymphocytic leukemia. A clear correlation between germline transcripts and HLA-DR expression was observed among germline-positive cases (p < 0. 01). C mu expression and response to therapy clearly indicated that germline-mu-positive leukemia patients responded poorly to chemotherapy and had a worse clinical prognosis compared with C mu-negative patients (p < 0.01). After two courses of chemotherapy, 7/9 C mu-negative patients achieved complete remission compared to only 7/29 C mu-positive patients (p < 0.01). We conclude that the gene-regulating immunoglobulin germline C mu may be amplified in myeloid and B-lymphoid cells during leukemogenesis. Such genetic changes may be correlated with cellular terminal differentiation injury, resistance to chemotherapy and uncontrolled malignant cell proliferation.
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PMID:Transcripts of immunoglobulin germline mu: an amplified myeloid and B-lymphoid common gene program in various leukemias. 1035 29

The MLL gene is fused with the cAMP-responsive element binding protein-binding protein (CBP) gene in t(11;16)(q23;p13), which has been reported to be associated with therapy-related acute leukemia. We established a novel myeloid cell line, SN-1, from a patient with T-cell acute lymphoblastic leukemia with t(11;16)(q23;p13) having in-frame MLL-CBP fusion transcripts. The majority of the SN-1 cells were positive for myeloperoxidase when examined using an electron microscope and expressed CD13, CD33, CD56, and HLA-DR antigens, but not CD7, CD10, CD19, CD34, or CD41 antigens, suggesting that these cells are of myeloid origin. SN-1 cells underwent functional and morphological differentiation when treated with actinomycin D or sodium butyrate, but not with all-trans-retinoic acid (ATRA) or 1alpha,25-dihydroxyvitamin D3 (VD3). Exposure of SN-1 cells to ATRA hardly affected cell growth and differentiation, whereas the growth of HL-60 and NB4 cells treated with ATRA was effectively inhibited, and differentiation into mature granulocytes was induced. SN-1 cells were relatively insensitive to VD3 with respect to inhibiting the cell growth and inducing the ability to reduce nitroblue tetrazolium, lysozyme activity, and morphological differentiation, although the expression of CD11b was slightly induced by VD3. These results suggest that the cell line was impaired in the signal transduction systems of ATRA and VD3. This cell line should be useful for the study of the role of CBP as a transcriptional regulator in leukemia differentiation and for the functional analysis of the MLL-CBP fusion gene, which will provide new insights into leukemogenesis caused by 11q23 translocations.
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PMID:SN-1, a novel leukemic cell line with t(11;16)(q23;p13): myeloid characteristics and resistance to retinoids and vitamin D3. 1070 36


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