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)

Most of the circulating lymphocytes from three asymptomatic adults (one male, two female, age range 61-67 years) with isolated persistent lymphocytosis of between 7.1 and 10 x 10(9)/l possessed characteristic villous projections of the cell membrane. Morphological, histochemical, ultrastructural, immunological, and genotypic studies confirmed a clonal proliferation of tartrate-resistant acid phosphatase (TRAP)-negative CD5-CD10-CD25- and CD11c+ B-cells. In addition to CD11c, these cells expressed other adhesion receptors (LFA-1/CD11a, VLA-4/CD29/49d, ICAM-1/CD54, and LAM-1) and produced detectable amounts of interleukin-1 beta, interleukin-6, and in one case tumour necrosis factor-alpha mRNA. This monoclonal villous lymphocytosis (MVL) could be differentiated from B-cell chronic lymphocytic, prolymphocytic, and hairy cell leukaemias, and from previously recognized CD11c+ chronic B-cell leukaemia. A rare splenomegalic non-Hodgkin's lymphoma variant with circulating villous B-lymphocytes (SLVL), usually CD10+ and sometimes CD11c- and TRAP+, appears to be a closely related disorder. In all three patients the lymphocyte count increased very slowly, at a rate less than 5 x 10(9)/l per year, over 3-7.5 years of follow up, and a moderate splenomegaly eventually developed in one of the patients. Chemotherapy was never required. MVL may be a relatively benign clinical entity akin to SLVL within the group of CD11c+ B-cell lymphoproliferative disorders.
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PMID:Monoclonal lymphocytosis with villous lymphocytes: a chronic lymphoproliferative disease of CD11c+ B-cells. 168 36

A case of splenic lymphoma with circulating villous lymphocytes is reported. Short surface cellular expansions were observed on blood and marrow films and by transmission electron microscopy. The immunophenotype was that of mature B cells without CD5, CD10, CD11c, or CD25 expression or tartrate-resistant acid phosphatase. Despite a basophilic plasmacytoid-like cytoplasm, this case of splenic lymphoma with circulating villous lymphocytes differed from splenic immunocytoma in that immunofluorescence and ultrastructure suggested that the neoplastic cells did not possess high levels of intracytoplasmic immunoglobulin. Treatment of cytopenia was best achieved by splenectomy and the total follow-up thus far (30 months) seems to indicate a case of low-grade malignant lymphoma.
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PMID:Splenic lymphoma with circulating villous lymphocytes. Report of a case with immunologic and ultrastructural studies. 172 57

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

A 55-year-old woman was first seen in October 1986, because of splenomegaly, moderate anemia and leukocytosis. The hemoglobin was 8.8 g/dl, platelet count 24.4 X 10(4)/microliters, and the white cell count 23,800/microliters with 73% atypical lymphoid cells. The bone marrow nucleated cell count was 99,000/microliters with 36% lymphoid cells. These atypical lymphoid cells showed hairy appearance under phase-contrast microscopy, and were positive for tartrate-resistant acid phosphatase. These cells showed the surface phenotype of CD10, CD19, CD20, Leu M5, HCM, and IgG K. Biochemical data revealed marked polyclonal hypergammagloburinemia (PHG) of IgG type (IgG 8756 mg/dl). To elucidate the mechanism of the PHG, we investigated whether hairy cells produce interleukin 6 (IL-6) and express IL-6 receptor. The culture supernatant of these hairy cells increased 3H-thymidine uptake of a IL-6 dependent hybridoma clone (MH60) in a dose-dependent manner. These cells were stained with anti-IL-6 antibody using immuno-cytochemical technique. Our results suggested that these hairy cells produce and secrete IL-6. Immunocytochemical staining with anti IL-6 receptor antibody and the binding assay with 125I-labelled recombinant IL-6 revealed that these cells express little or no receptors for IL-6. It was therefore suggested that IL-6 produced by hairy cells in this case is not an autocrine growth factor for these cells but may play a role in development of PHG by stimulating normal B lymphocytes to produce an excessive amount of immunoglobulin.
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PMID:[Production and secretion of BSF2/IL6 in a case of hairy cell leukemia with polyclonal hypergammaglobulinemia]. 238 10

Bryostatin 1 (Bryo1), a macrocyclic lactone and a protein kinase C activator, is extracted and purified from the marine bryozoan Bugula neritina. In this study we describe its effect on morphology, surface immunophenotype, acid phosphatase (AcP), tartrate-resistant acid phosphatase (TRAP), proliferation and cell cycle of non-Hodgkin's B-lymphoma cell lines representing four differentiation stages. Except for the WSU-BL, a high-grade SCNCL, all other cell lines showed obvious changes in their morphology when treated with 200 nM Bryo1. Phenotypically, a dramatic decrease of CD10 and induction of CD11c and BL7 on some cell lines consistent with further B-cell differentiation was seen. The lines in control cultures showed variable expression of AcP and TRAP. Following treatment with Bryo1, there was a general increase in AcP expression except in WSU-BL line. WSU-FSCCL and WSU-DLCL were TRAP-negative but became TRAP-positive when treated with Bryo1. Cell growth and cycle analysis during treatment of different cell lines revealed evidence of strong, moderate, or no growth inhibition by Bryo1 compared with control cultures. Our results indicate that Bryo1 shows differentiation effects on low-grade FSCCL, intermediate-grade FLCL and high-grade DLCL, and stimulatory or no effect on high-grade SCNCL. Since Bryo1 does not have tumor-promoting activity, it has a potential therapeutic role as a B-cell differentiating agent.
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PMID:Differential effects of bryostatin 1 on human non-Hodgkin's B-lymphoma cell lines. 842 74

Splenic marginal zone cell lymphoma (SMZCL) is a recently described clinicopathologic entity, that is reported to overlap with splenic B-cell lymphoma with villous lymphocytes. The authors describe the clinicopathologic, immunophenotypic, and molecular findings in five cases of SMZCL. There were two males and three females, with a mean age of 68.4 years, who presented with peripheral blood cytopenias and splenomegaly. One patient had an absolute lymphocytosis with many villous lymphocytes. With clinical follow-up of 9 to 37 months, two patients are alive and three patients died of unrelated causes. Splenectomy was done in each patient and the spleens were large, 970-2,400 g. Histologically, the SMZCLs preferentially replaced the marginal and mantle zones with partial or complete replacement of germinal centers in the white pump. The neoplastic cells were predominantly small to medium in size with oval or slightly irregular nuclei and relatively abundant pale or eosinophilic cytoplasm. Immunophenotypic studies demonstrated that the neoplastic cells expressed monotypic immunoglobulin, IgD in four tumors, pan-B-cell antigens, and bcl-2. The tumor cells were negative for the CD2, CD3, CD5, CD10, CD11c, CD25, CD35, CD38, CD45RO, and CD68 antigens, and tartrate-resistant acid phosphatase. Southern blot hybridization revealed immunoglobulin gene rearrangements in all tumors. The major breakpoint region of the bcl-2 gene and the T-cell receptor beta chain gene were in the germline configuration. Polymerase chain reaction studies did not identify the t(14;18) or t(11;14). All cases were negative for p53 protein and single-stranded conformational polymorphism analysis for p53 gene mutations was negative. Our results support the concept that SMZCL is a clinically indolent, low grade B-cell lymphoma that probably arises from splenic marginal zone lymphocytes.
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PMID:Splenic marginal zone cell lymphoma. An immunophenotypic and molecular study of five cases. 860 7

A cell line, JHC-2, was established from the peripheral blood of a patient with hairy cell leukemia (HCL)-Japanese variant. The JHC-2 cells have cytologic features similar to those of the original tumor cells. They displayed hairy cytoplasmic projections by phase contrast and scanning electron microscopy. The tartrate-resistant acid phosphatase reaction was weakly positive. The immunophenotype of the JHC-2 cells was CD5-, CD10-, CD11c+/-, CD19+, CD21+, CD23+, CD24-, CD25+/-, CD38- and FMC-7+. The expression of surface immunoglobulin (IgG, kappa) and the configuration of Ig gene rearrangements in the JHC-2 cells were identical to those in the original leukemic cells, and the JHC-2 cells displayed trisomy 9 on cytogenetic examination. Southern blot analysis for the Epstein-Barr virus (EBV) genome showed that the JHC-2 cells contained the EBV genome, although the freshly isolated leukemic cells did not. These results indicate that the JHC-2 cell line is an EBV spontaneously transformed B cell line originating from HCL cells.
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PMID:Establishment of a new cell line from a patient with hairy cell leukemia-Japanese variant. 916 47

We report a 70-year-old Japanese man who had splenic lymphoma with villous lymphocytes and a complex chromosomal abnormality. No monoclonal gammopathy was present. The peripheral blood film showed lymphocytes with thin and short villi arising from one or two poles of the cells. These cells were negative for tartrate-resistant acid phosphatase stain. Immunophenotyping of peripheral blood lymphocytes showed moderate to strong expression of surface membrane IgM, IgD, IgA, and lambda as well as CD19, CD20, CD21, CD24, and HLA-DR. In addition, there was weak CD5, CD22, and CD25 expression, but no CD10, CD11c, CD23, CD38, or B-ly-7 expression. All 20 metaphases obtained from peripheral blood cells cultured for 5 days with lipopolysaccharide showed an abnormal karyotype: 47, XY, +der(3) t(3; 13) (q26; q12) inv(3) (?), t(7; 14), (q21; q11), der(13) t(3; 13) (q26; q12). Our patient followed a relatively benign clinical course and splenectomy was not performed.
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PMID:[Splenic lymphoma with villous lymphocytes and complex chromosomal abnormality]. 924 32

An 88-year-old Japanese woman with splenomegaly, but without lymphadenopathy, was admitted because of epigastric distress. Laboratory data disclosed an RBC of 310 x 10(4)/microliter, Hb of 10.1 g/dl, Ht of 30.6%, Plt count of 9.8 x 10(4)/microliter, and WBC of 4,470/microliter with 38% abnormal lymphocytes. Peripheral blood films revealed lymphocytes with thin, short cytoplasmic villi, condensed nuclear chromatin, and small nucleoli. The lymphocytes stained negative for tartrate-resistant acid phosphatase. Also, immunophenotyping was positive for expression of the cell surface markers CD19, CD20, IgG, kappa and HLA-DR, but not for CD5, CD10, CD11c, CD23, CD25, CD38, or CD103 antigens. Chromosomal analysis of peripheral blood cells disclosed the 46, XX, del(7), (q32) aberration. A splenectomy was performed simultaneously with partial colon resection because of a mucinous carcinoma found in the transverse colon. Histologic examination of resected spleen tissues revealed a distinctive pattern of white pulp infiltration by lymphoma cells. The histologic findings and clinical data were consistent with the features of splenic lymphoma with circulating villous lymphocytes. Our patient exhibited a relatively benign clinical course, and was being followed on an outpatient basis with no additional therapy.
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PMID:[Splenic lymphoma with villous lymphocytes expressing chromosomal abnormalities]. 1035 43

A 67-year-old male was admitted because of lymphocytosis and huge splenomegaly. Abnormal lymphocytes had cytoplasmic hairy projections and were negative for tartrate-resistant acid phosphatase staining. The bone marrow aspirate contained many lymphocytes with the same morphology. Flow cytometric analysis revealed an increase in IgM and kappa positive B cells. They were positive for CD11c, CD19, CD20 and FMC7, and negative for CD5, CD10 and CD25. The patient was diagnosed as having hairy cell leukemia, Japanese variant. Initially interferon-alpha was administered for a month, decreasing the numbers of leukemic cells but with little effect on splenomegaly. Subsequent administration of cladribine (0.09 mg/kg, 7 days) showed a remarkable effect, and the patient has been in complete remission for 8 months.
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PMID:[Hairy cell leukemia, Japanese variant, successfully treated with cladribine]. 1519 52


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