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)

Peripheral blood mononuclear cells from 24 patients with prolymphocytic leukemia (PLL) were isolated using a Ficoll-Hypaque gradient and stained by indirect immunofluorescence using a wide panel of monoclonal antibodies against B cell restricted and associated antigens, including HLA DR (Ia), CD19, CD21 (C3dR) surface membrane immunoglobulin (Slg), CD10 (CALLA), C3b, B5, CD25 (TAC), PCA1, T9, and T10. The cells were also tested for the FMC7, defined previously on PLL cells and the RAB1, a newly described hairy cell leukemia antigen. Thirteen out of the 24 samples expressed with variable intensity all the above antigens. While Ia, CD19, CD20, FMC7, and RAB1 were strongly or moderately expressed in all, the complement receptors (CD21 and C3b) were only weakly expressed in 12 cases; and the activation antigens B5, TAC, T9, T10, and PCA1 were found with variable intensity in two-thirds of the cases. In 50% of the cases tested, the CD5 antigen (usually strongly expressed on B CLL cells) was weakly to moderately expressed. These findings (absence or weak expression of complement receptors with variable expression of activation antigens) suggest that the PLL cells are activated B cells. When stimulated in vitro by anti-mu and TPA, (phorbol ester) tumor cells showed a decrease in CD21 and Slg and a stronger expression of CD25, T9, T10, and PCA1, with evidence of Ig secretion in four out of the seven cases studied. This confirms that the PLL cells arrested at an advanced stage of differentiation progressed narrowly to more differentiated cells. In view of our findings, we believe that the term prolymphocytic leukemia is inaccurate to define the stage of cell differentiation, and we suggest calling the disease preplasmacytic leukemia.
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PMID:Further characterization of prolymphocytic leukemia cells as a tumor of activated B cells. 984 Sep 14

We describe the clinical and laboratory features of 17 adult patients with a variant form of hairy cell leukemia (HCL-V) studied over the last 7 years. The main findings were: splenomegaly, moderate anemia, thrombocytopenia, and a raised white blood cell count (median 116 x 10(9)/L; range 15 to 482). The circulating lymphoid cells had abundant villous cytoplasm and a round, occasionally bilobed nucleus, with a prominent nucleolus. Monocytopenia, a feature of typical HCL, was not seen; neither was tartrate-resistant acid phosphatase demonstrated in eight cases tested. HCL-V cells had a mature B-cell phenotype: CD19+, CD20+, CD22+, FMC7+, CD11c+, CD10-, CD5-, with light chain isotope restriction in 15 cases. In contrast to typical hairy cells, HCL-V cells were negative with the monoclonal antibodies anti-HC2 and anti-TAC (CD25). Immunoglobulin (Ig) was not detected in two cases and IgG was expressed in the cell membrane of 73% of cases. Bone marrow histology was different from HCL, showing interstitial infiltration by cells clumped together and a moderate amount of reticulin, but the spleen showed the typical red pulp expansion of HCL. HCL-V patients did not respond to splenectomy (5 of 7) or alpha-interferon (7 of 7); 2 of 3 patients had a partial response to 2'deoxycoformycin. The clinical course was benign with 15 patients alive with a median survival greater than 4 years. We confirm that HCL-V is a distinct clinico-pathologic entity with intermediate features between HCL and B-prolymphocytic leukemia.
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PMID:A variant form of hairy cell leukemia resistant to alpha-interferon: clinical and phenotypic characteristics of 17 patients. 236 67

Leukemic cells of a 19 year old patient with prolymphocytic leukemia of T-cell type (T-PLL) were characterized by surface markers and immunologic functions. Phenotypic analysis using a large panel of monoclonal antibodies corresponding to the clusters (CD) of differentiation antigens established on the Leukocyte Typing Workshops I and II revealed a unique T-cell phenotype not yet reported in the literature: CD1 (T6)-, CD2 (T11)+, CD3 (T3)+, CD4 (T4)-, CD5 (T1)-, CD6 (T411)+, CD7 (Leu9)+, CD8 (T811)-, CD10 (J5)-, CD11 (M22)+, CD12 (M67)-, CD13 (My7)-, CD14 (Mo2)-, CD16 (Vep13, 3G8, Leu11)+, CD18 (MHM23)+, CD19 (B4)-, CD20 (B1)-, CD25 (TAC)-, MHC-class II (HLA-DR, HLA-DQ)-, NKH1A+, Leu7-. Despite the expression of surface structures associated with natural killer (NK) function (CD16, CD18, NKH 1 A) the T-PLL cells were inactive in NK assays in vitro. Low in vitro ADCC activity was detectable. This unusual T-PLL phenotype might help to identify a new distinct T-cell differentiation stage.
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PMID:T-cell prolymphocytic leukemia (T-PLL) with unique surface phenotype. 310 23