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)

We describe here two patients with mantle cell lymphoma (MCL) who after a few years, developed to the diffuse large cell lymphoma (DLCL) (anaplastic centrocytic lymphoma) growing in a diffuse sheets without the classical MCL component. In both the initial and second biopsy specimens, in each case, tumor cells were positive for cyclin D1, sIgM, sIgD, and CD5, but were negative for CD10 and CD23. In a study of immunoglobulin heavy chain (IgH) gene rearrangement, using the polymerase chain reaction (PCR) method, the products obtained from each paired biopsy tissue sample were the same size, and in one case had an identical sequence to the non-mutated VH gene. Immunohistochemistry was used to examine the expression of p53, p27Kip1 and cyclin E. Interestingly, there was clear overexpression of p53 protein in case 1 but not in case 2, compared with other typical MCL cases. The expression of p27Kip1 in the second biopsies of each case was decreased compared with those in the initial biopsies. In case 2, however, p27Kip1 was clearly expressed in the first and second biopsies, in contrast to other typical MCL cases. Thus these 2 cases demonstrate not only that the variant form of MCL may arise de novo, but also that MCL may transform to DLCL at the time of relapse. Although the mechanism of tumor progression/transformation is still poorly understood, the overexpression of p53 or p27Kip1 may be linked to a cellular mechanism involved in the development of the variant form of MCL.
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PMID:Expression of cell cycle regulating proteins in an unusual transformation of mantle cell lymphoma. 1061 57

We previously reported that decidual stromal cells (DSC) from early human decidua express antigens associated with hematopoietic cells and develop different immune functions. Here we study the antigenic phenotype of DSC from term decidua and compare it with the phenotype reported for DSC from early decidua. Decidual stromal cells were isolated from human term deciduas and maintained in culture until highly purified DSC cultures were obtained. Most term DSC, like most early DSC, expressed CD10. Term DSC expressed antigens specific for follicular dendritic cells (FDC), such as DRC-1 (CD21L) and HJ2, together with CD21, CD23 and CD80, which are detected on FDC as well. Also like early DSC, term DSC were negative for CD3, CD14, CD15 and CD45. Although early DSC were reported to be HLA-DR-positive and CD86-positive, these antigens were not expressed by term DSC. These discrepant results suggest that two types of cells, or cells at different stages of differentiation (decidualization) were selected during culture of decidual cells from different periods of gestation. This possibility was further supported by the finding that term DSC expressed desmin and prolactin, two markers of decidualization, whereas these molecules have not previously been detected in early DSC.
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PMID:Antigen phenotype of cultured decidual stromal cells of human term decidua. 1066 Feb 60

The aim of this study was to establish how effective is the use of immunohistochemistry on formalin-fixed bone marrow in diagnosing low-grade B-cell neoplasms. We investigated a series of 41 consecutive patients with bone marrow involvement for whom no other diagnostic tissues were available. The sections were stained with the following antibodies: CD3, CD20, CD79a, CD5, CD10, CD23, anti-cyclin D1 and kappa and lambda light chains. Antigen retrieval was performed using either a microwave oven or a pressure cooker. Labelling was performed with an avidin-biotin-peroxidase labelling system. A final diagnosis was reached in 37 out of 41 cases (90%): B-chronic lymphocytic leukaemia (15 cases), follicular lymphoma (10 cases), mantle-cell lymphoma (eight cases) and lymphoplasmacytoid lymphoma/immunocytoma (four cases). In the remaining four cases, a generic diagnosis of low-grade B-cell neoplasm was made. The immunophenotyping of formalin-fixed marrow is a useful technique for diagnosing most of the low-grade B-cell neoplasms.
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PMID:The diagnosis of low-grade peripheral B-cell neoplasms in bone marrow trephines. 1069 67

Marginal zone B-cell lymphoma (MZL) is a recently individualized lymphoma that encompasses mucosa-associated lymphoid tissue (MALT) lymphoma, splenic lymphoma with or without villous lymphocytes, and nodal lymphoma with or without monocytoid B-cells. If the clinical description and outcome of MALT lymphoma is well known, this is not the case for the other subtypes. We reviewed 124 patients presenting non-MALT MZL treated in our department to describe the morphologic and clinical presentation and the outcome of these lymphomas. Four clinical subtypes were observed: splenic, 59 patients; nodal, 37 patients; disseminated (splenic and nodal), 20 patients; and leukemic (not splenic nor nodal), 8 patients. These lymphomas were usually CD5-, CD10-, CD23-, and CD43-, but the detection of one or, rarely, two of these antigens may be observed. Bone marrow and blood infiltrations were frequent, except in the nodal subtype, but these locations were not associated with a poorer outcome. Splenic and leukemic subtypes were associated with a median time to progression (TTP) longer than 5 years, even in the absence of treatment or of complete response to therapy. Nodal and disseminated subtypes were associated with a median TTP of 1 year. However, in all these subtypes, survival was good with a median survival of 9 years, allowing these lymphomas to be classified as indolent. Because of the retrospective nature of this analysis, no conclusion may be drawn on the therapeutic aspects, but conservative treatments seem recommended for leukemic and splenic subtypes. (Blood. 2000;95:1950-1956)
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PMID:Non-MALT marginal zone B-cell lymphomas: a description of clinical presentation and outcome in 124 patients. 1070 60

Besides the problems inherent in endoscopically obtained tissue and the low incidence of intestinal lymphomas, the major difficulties reside in the distinction to reactive processes and in the differential diagnosis among several lymphoma entities. Knowledge of the microanatomical and biological properties of the intestinal MALT, supplemented by sufficient clinical information, are important prerequisites for the diagnostic work-up which has to include immunohistochemical studies. Whereas the diagnosis of aggressive B-cell lymphomas (diffuse large B-cell lymphoma, Burkitt's lymphoma) is usually straightforward, lymphomatous polyposis (LP, the intestinal equivalent of mantle cell lymphoma) and low-grade B-cell lymphoma of MALT-type may be difficult to diagnose and to separate from reactive lymphoproliferations. The characteristic immunohistochemical profile of LP (cyclin D1 + CD5 + CD43 + CD23 - CD10 - IgM kappa or lambda, is very helpful in this regard and similarly useful to exclude intestinal involvement by B-CLL or follicular center lymphoma. In addition, the endoscopic appearance characterized by seeds of small polyps along the colorectum favors LP although MALT-type lymphoma may occasionally produce polypoid lesions. Focal lymphoid hyperplasia occurs in the terminal ileum and may present with a mass in the right iliac fossa. The diagnosis of intestinal T-cell lymphoma (ITL) represents the most challenging task for both clinicians and pathologists. This disease is often associated with and may closely mimick celiac disease of adult onset type, or can be misdiagnosed as inflammatory bowel disease. The presence of an abnormal activated T-cell phenotype, i.e. different from that of normal intraepithelial lymphocytes, strongly suggests ITL and is of particular importance in cases that lack overt cytological atypia.
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PMID:[Problems in biopsy differential diagnosis in lymphomas of the small and large intestines]. 1071 99

To our knowledge, blastic transformation of splenic marginal zone lymphoma, a recently characterized low-grade lymphoproliferative disorder, has not been reported previously. In this regard, we report the unique case of a 70-year-old woman whose untreated splenic marginal zone lymphoma underwent blastic transformation 3 years after diagnosis. Her hematologic medical history started in 1988 as thrombocytopenia refractory to steroids associated with atypical lymphoid infiltrate in the bone marrow. She underwent splenectomy in 1989, which revealed splenic marginal zone lymphoma. One year later, the patient developed lymphadenopathy noted in the chest, axillary, abdominal, and retroperitoneal lymph nodes. Because she was asymptomatic, treatment was limited to a conservative supportive regimen. The nodal lymphoma cells had features associated with marginal zone lymphoma and expressed B-cell monotypic kappa light chain. She was readmitted for the last time 2 years later with findings of 16% blasts in the peripheral blood and massive infiltration of the bone marrow by large blastoid cells. The blasts showed dispersed chromatin and prominent nucleoli, and possessed a moderate amount of clear cytoplasm. The blasts, like the previous nodal and splenic lymphomas, had a CD20-, CD19-, IgM-positive phenotype, but lacked reactivity for CD5, CD10, and CD23. The patient displayed clinical remission after treatment with vincristine and prednisone, but died of aspiration pneumonia 1 month later. These observations suggest that, similar to the other low-grade lymphoproliferative disorders, an untreated splenic marginal zone lymphoma may undergo high-grade blastic transformation.
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PMID:Blastic transformation of splenic marginal zone B-cell lymphoma. 1078 61

Immunophenotypic analysis is critical in categorizing small B-cell neoplasms; however, many recommended antibody panels have required fresh or frozen tissue. Many paraffin-reactive antibodies are now available but have been studied mostly in isolation. Therefore, the utility of a panel of paraffin-reactive antibodies in differentiating small B-cell neoplasms was investigated. Paraffin-embedded sections of small lymphocytic lymphoma/B-chronic lymphocytic leukemia (SLL/B-CLL; 12), mantle cell (MCL; 15), follicular (FL; 11), and marginal zone B-cell (MZL; eight) lymphomas were stained with CD20/L26, CD3, CD43/DF-T1 or Leu22, CD5/4C7, CD23/BU38, cyclin D1/H295, and CD10/56C6 antibodies. For select antibodies, results were compared to flow cytometric data (FC). Formalin and B5 fixation were also compared. Seven of 11 SLL/B-CLL were CD43+ CD5+ CD23+ cyclin D1- CD10-; seven of 11 MCL were CD43+ CD5+ CD23- cyclin D1+ CD10-; nine of 10 FL were CD43- CD5- CD23- cyclin D1- CD10+; and five of six MZL were CD43+ CD5- CD23- cyclin D1- CD10-. CD5, CD23, and CD10 stains showed sensitivities of 81, 88, and 100%, respectively, compared to FC. With B5 fixation, cyclin D1 was more often negative and CD5 more often equivocal. A panel of paraffin-reactive antibodies aids in classification of small B-cell neoplasms, although a small number of cases have indeterminate phenotypes and MZL have no defining features. CD5 separates most SLL/B-CLL and MCL from FL and MZL. CD23 separates SLL/B-CLL from most MCL, but cyclin D1 is most important for identifying MCL. CD10 positivity distinguishes most FL from other small B-cell lymphoid neoplasms.
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PMID:Classification of small B-cell lymphoid neoplasms using a paraffin section immunohistochemical panel. 1093 42

In May, 1998, a 63-year-old woman was admitted for treatment of relapsed malignant lymphoma. In March 1997, a diagnosis of diffuse large B-cell lymphoma(DLBL), clinical stage IIISE A, was made from a biopsy specimen of the tumor in the left buccal mucosa. Six cycles of CHOP regimen were given, and complete remission was achieved. However, relapse of the lymphoma was suspected, and the patient was transferred to our hospital. On admission, a right tosillar mass, 8 mm in diameter, was found, and a biopsy showed DLBL. The immunophenotype of the lymphoma cells was CD3- CD4- CD5- CD8+ CD10- CD19+ CD20+ CD23- CD25+ IgL (lambda)+, and dual staining confirmed that the cells were CD8+ and CD19+. The patient was an HTLV-1 carrier, but monoclonal integration of HTLV-1 proviral DNA into the lymphoma cells was not detected. She was diagnosed as having CD8+ DLBL, clinical stage IA. Because she responded to salvage chemotherapy, autologous peripheral blood stem cell transplantation was performed and complete remission was obtained. To our knowledge, this is the first report of CD8+ DLBL.
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PMID:[CD8-positive diffuse large B-cell lymphoma]. 1102 Sep 83

We report an unusual case of Epstein-Barr virus (EBV)-associated mucosal-associated lymphoid tissue (MALT) lymphoma involving the lungs, kidneys, and axillary lymph nodes in a child with congenital hypoadrenalism and panhypopituitarism. The patient presented with an aggressive clinical course and histologic evolution. Initial biopsies (1994) of the lung and kidney revealed histologic features of low-grade B-cell MALT lymphoma with lymphoepithelial lesions within the renal tubules and bronchial epithelium. Subsequent biopsies (1996, 1997, and 1999) revealed progressively greater cytologic atypia, polymorphism, and necrosis; an increased mitotic rate; and a preponderance of large cells, indicative of progression from a low-grade to a high-grade MALT lymphoma. Immunophenotyping of the lung and lymph node lesions revealed identical surface marker profiles: cells were CD19(+), CD20(+), immunoglobulin (Ig) G(+), kappa(+), lambda(-), CD5(-), CD10(-), CD23(-), and IgM(-), and also negative for T-cell markers. Genotypic analysis demonstrated the presence of immunoglobulin heavy chain rearrangement and monoclonality of EBV in the lung lesion by Southern blot hybridization and polymerase chain re()action (PCR). The clinicopathologic features suggest that these lesions might represent an immunosupression-related continuum of low-grade to high-grade MALT lymphomas. Infection with EBV may have contributed to this tumor's aggressive clinical and histologic evolution.
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PMID:Epstein-Barr virus-associated high-grade B-cell lymphoma of mucosal-associated lymphoid tissue in a 9-year-old Boy. 1103 88

We describe here two patients with mantle cell lymphoma (MCL) who after a few years, developed to the diffuse large cell lymphoma (DLCL)( anaplastic centrocytic lymphoma) growing in a diffuse sheets without the classical MCL component. In both the initial and second biopsy specimens, in each case, tumor cells were positive for cyclin D1, sIgM, sIgD, and CD5, but were negative for CD10 and CD23. In a study of immunoglobulin heavy chain (IgH) gene rearrangement, using the polymerase chain reaction (PCR) method, the products obtained from each paired biopsy tissue sample were the same size, and in one case had an identical sequence to the non-mutated VH gene. Immunohistochemistry was used to examine the expression of p53, p27(Kip1) and cyclin E. Interestingly, there was clear overexpression of p53 protein in case 1 but not in case 2, compared with other typical MCL cases. The expression of p27(Kip1) in the second biopsies of each case was decreased compared with those in the initial biopsies. In case 2, however, p27(Kip1) was clearly expressed in the first and second biopsies, in contrast to other typical MCL cases. Thus these 2 cases demonstrate not only that the variant form of MCL may arise de novo, but also that MCL may transform to DLCL at the time of relapse. Although the mechanism of tumor progression/transformation is still poorly understood, the overexpression of p53 or p27(Kip1) may be linked to a cellular mechanism involved in the development of the variant form of MCL.
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PMID:Expression of Cell Cycle Regulating Proteins in an Unusual Transformation of Mantle Cell Lymphoma. 1104 6


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