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)

Previously, we have shown that nuclear envelope assembly in cell-free extracts of Xenopus eggs requires two distinct vesicle-containing fractions, called Nuclear Envelope Precursor Fractions A and B (NEP-A and NEP-B). These fractions are characterized further in this paper and the manner in which they are regulated during metaphase is examined. Antisera against the NEP-B fraction recognized several proteins common to NEP-B and Xenopus oocyte or liver nuclei, but not to NEP-A or cytosol. A known glycoprotein component of the nuclear pore complex, p62, also co-fractionated with NEP-B, whereas the Xenopus egg lamin LIII did not. Together, these results provide further evidence that the NEP-B fraction contains precursors of the nuclear envelope. The regulation of NEP-A and -B function during metaphase, when the nuclear envelope is disassembled, was examined by treating each fraction with metaphase cytosol or purified protein kinase preparations isolated from metaphase-arrested eggs. Treatment of NEP-B with metaphase cytosol, under conditions where proteins are irreversibly phosphorylated, inhibited the subsequent assembly of the nuclear envelope by preventing the binding of NEP-B to chromatin. In contrast, similar treatment of NEP-A did not affect its ability to form nuclear envelopes. The changes in NEP-B during metaphase did not appear to be regulated directly by either p34cdc2/cyclin B, S6 kinase II or MAP kinase.
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PMID:Regulation of nuclear envelope precursor functions during cell division. 140 Jun 33

Lymph nodes from 21 cases of malignant lymphoma of a centrocytic (mantle cell) type, (ML, cc (mc)) were examined. All the cases had monoclonal surface immunoglobulin (sig) M and/or D, but were negative for CD10 (CALLA), and CD11c (LeuM5). Lymphoma cells with CD25 (anti-Tac)+, CD5 (Leu1)+, and alkaline phosphatase (ALPase)- in eight cases showed bone marrow involvement (10-66% of the nucleated cells; mean 32 +/- 18%) but with no leukemic changes. These eight cases had a similar phenotype and were distributed by the lymphoma cells to the examined B-chronic lymphocytic leukemia. Seven cases showed an infiltration of CD25-, CD5+, and ALPase- lymphoma cells, in which only two cases showed focal bone marrow involvement. There was a close relationship between CD25 expression and bone marrow invasion by the lymphoma cells in ML, cc (mc). Three of the six CD25- and CD5- cases presented zonal proliferation of ALPase+ lymphoma cells with round nuclei and a high anti-proliferating cell nuclear antigen/cyclin (PCNA/c) rate in the mantle zone and paracortex, accompanied by a prominent interdigitating dendritic and histiocytic cell reaction. Examined CD25-, CD5- and ALPase+ lymphoma showed a neoplastic counterpart of so-called marginal zone lymphocytes, which was different from other cases of ML, cc (mc). Lymphoma cells in ML, cc (mc), except for those of the so-called marginal zone lymphoma, might be derived from slgM+, D+/-, CD25+/-, CD5+/-, ALPase-, CD10- and CD11c- lymphocytes present in the mantle zone and primary lymph follicles.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinicopathologic, enzyme and histochemical studies of centrocytic (mantle cell) lymphoma: comparison with other types of low-grade B cell lymphoma based on the updated Kiel classification. 832 10

Mantle-cell lymphoma comprises 2%-10% of all non-Hodgkin's lymphomas (NHLs). Patients present with generalized disease, and have a poor prognosis. Three different histologic patterns (mantle zone, nodular, and diffuse) and three different cytological variants (classical, blastic, and pleomorphic) have been described. The phenotype (strong surface IgM, CD5+, CD10-, CD23-, cyclin D1+ and B-cell markers+) is remarkably constant. Dependent on the methods used (PCR, Southern blot analysis, and cytogenetics) a t(11;14) can be detected in approximately 35%-66% of cases. Using FISH analysis, possibly almost all cyclin D1-expressing MCLs carry this translocation, indicating that a substantial part of these translocations are missed by conventional methods. This has been confirmed by DNA fiber FISH analysis by which the breakpoints could be accurately mapped over a 220 kb region centromeric of the cyclin D1 gene. Additional genetic abnormalities involve breakpoints and deletion at the 3' end of the cyclin D1 gene, numerical chromosomal aberrations, mutations in p53, and deletions of p16. These may be associated with tumor progression. Owing to the translocation t(11;14), the cyclin D1 gene is activated. At the RNA level, approximately 90% of MCLs show overexpression. This corroborates immunohistochemistry on paraffin tissue sections. Since expression of cyclin D1 in normal lymphoid cells is very low to undetectable, and only hairy-cell leukemia and very few other B-cell lymphomas show expression, immunohistochemistry for cyclin D1 provides an excellent marker for MCL. In hairy-cell leukemia, expression is moderate and cannot be explained by chromosomal translocation.
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PMID:Bcl-1/cyclin D1 in malignant lymphoma. 920 53

Mantle cell lymphomas comprise 2 to 8% of non-Hodgkin's lymphoma in the United States. They occur in older adults with a distinct male predominance, who present with generalized lymphadenopathy, and often have disseminated disease at the time of diagnosis. Pathologically, mantle cell lymphomas are characterized by a proliferation of small lymphocytes, with irregular nuclei, clumped chromatin, and sparse cytoplasm that can grow in nodular or diffuse patterns in lymph nodes, that localize to the splenic white pulp and that produce interstitial, paratrabecular, and intertrabecular lymphoid aggregates in the bone marrow. Phenotypically, mantle cell lymphomas are B cell neoplasms that express pan B cell lineage antigens, CD5 and CD43, and that are negative for CD10 and CD23. On a genetic level, many cases of mantle cell lymphomas have the t(11;14)(q13;q32) that causes overexpression of cyclin-D1, a protein that can be demonstrated by immunohistochemistry in many examples of mantle cell lymphoma and that can be exploited diagnostically to distinguish mantle cell lymphomas from other low-grade B cell lymphoproliferative disorders. The differential diagnosis of mantle cell lymphoma includes small B cell lymphoma, lymphoplasmacytic lymphoma, nodal, extranodal, and splenic marginal zone lymphomas, and follicular small cleaved cell lymphoma. In most instances, these disorders can be separated from one another by morphology, distinctive immunophenotypic profiles, and genetic features.
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PMID:Mantle cell lymphoma. 1009 79

Multiple lymphomatous polyposis (MLP) is characterized by multiple polyps involving long segments of the gastrointestinal (GI) tract. MLP is thought to represent mantle cell lymphoma (MCL) of the GI tract; however, some cases of follicular lymphoma (FL) of the GI tract are found with a multiple polypoid appearance. In the present study, to clarify the cellular origin of MLP, clonal immunoglobulin heavy chain (IgH) gene rearrangement of four cases with MLP was amplified by polymerase chain reaction (PCR) and analyzed for the presence of somatic mutation. The IgH variable (VH) region sequences of three cases (CD5+ CD10- cyclin D1+) showed a little somatic mutation compared with the closest published germline. The other case (CD10+ CD5- cyclin D1-) was highly mutated and showed intraclonal heterogeneity (ongoing somatic hypermutation). These data indicate that three of the cases with MLP are derived from pregerminal center B cells (mantle zone B cells) and one case with MLP from germinal center B cells. Our study suggests that MLP is a heterogenous group that includes MCL and FL.
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PMID:Multiple lymphomatous polyposis of the gastrointestinal tract is a heterogenous group that includes mantle cell lymphoma and follicular lymphoma: analysis of somatic mutation of immunoglobulin heavy chain gene variable region. 1033 31

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

Intestinal mantle cell lymphoma characteristically produces multiple polyps, a finding reported as multiple lymphomatous polyposis. The early stages of intestinal mantle cell lymphoma before polyp formation and the pattern of initial lymph node invasion, however, have not been described. We recently encountered two cases of intestinal mantle cell lymphoma in their early development found incidentally associated with advanced colonic adenocarcinoma. We present herein the clinical, histopathological, immunohistochemical, and molecular genetic features of these two cases. In one case, a single polypoid mass was found with invasion limited to mucosa and submucosa of the terminal ileum and without lymph node compromise. In the second case, there were multiple mucosal aggregates of neoplastic cells without formation of polyps. Regional lymph nodes in the latter case showed either partial or complete involvement by lymphoma. In both cases, immunohistochemistry (CD20+, CD5+, cyclin D1+, CD10-, and CD23-), and demonstration of clonal immunoglobulin heavy chain and bcl-1 gene rearrangements by PCR analysis confirmed the diagnosis of mantle cell lymphoma.
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PMID:Early phase of intestinal mantle cell lymphoma: a report of two cases associated with advanced colonic adenocarcinoma. 1150 42

To determine the possible role of the epigenetic mechanisms in carcinogenesis of the hepatocellular carcinoma, we methylation-profiled the promoter CpG islands of twenty four genes both in HCC tumors and the neighboring non-cancerous tissues of twenty eight patients using the methylation-specific PCR (MSP) method in conjunction with the DNA sequencing. In comparison with the normal liver tissues from the healthy donors, it was found that while remained unmethylated the ABL, CAV, EPO, GATA3, LKB1, NEP, NFL, NIS and p27KIP1 genes, varying extents of the HCC specific hypermethylation were found associated with the ABO, AR, CSPG2, cyclin a1, DBCCR1, GALR2, IRF7, MGMT, MT1A, MYOD1, OCT6, p57KIP2, p73, WT1 genes, and demethylation with the MAGEA1 gene, respectively. Judged by whether the hypermethylated occurred in HCC more frequently than in their neighboring normal tissues, the hypermethylation status of the AR, DBCCR1, IRF7, OCT6, and p73 genes was considered as the event specific to the late stage, while that the rest that lacked such a distinguished contrast, as the event specific to the early stage of HCC carcinogenesis. Among all the clinical pathological parameters tested for the association with, the hypermethylation of the cyclin a1 gene was more prevalent in the non-cirrhosis group (P=0.021) while the hypermethylated p16INK4a gene was more common in the cirrhosis group (P=0.017). The concordant methylation behaviors of nineteen genes, including the four previously studied and their association with cirrhosis has been evaluated by the best subgroup selection method. The data presented in this report would enable us to shape our understanding of the mechanisms for the HCC specific loss of the epigenetic stability of the genome, as well as the strategy of developing the novel robust methylation based diagnostic and prognostic tools.
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PMID:Methylation profiling of twenty four genes and the concordant methylation behaviours of nineteen genes that may contribute to hepatocellular carcinogenesis. 1467 55

Characteristically, mantle cell lymphoma (MCL) expresses surface immunoglobulin (sIg), CD19, CD20, and CD5 and lacks CD10 and CD23. Rare CD5-MCL variants have been described. This report describes a case of leukemic MCL with morphologically and immunophenotypically distinct classic MCL and blastoid-variant MCL (BV-MCL) components. The classic MCL had typical morphologic features and immunophenotype (kappa sIg light chain-restricted and CD5+; CD10- and CD23-). The BV-MCL had larger nuclei and open chromatin; these cells also were kappa sIg light chain-restricted; however, they were CD10+ and CD5-. Fluorescence in situ hybridization studies demonstrated cyclin D1-immunoglobulin heavy chain gene fusion in both components; the bone marrow biopsy cellularity was replaced by CD10+ and cyclin D1+ and CD5-BV-MCL. This case illustrates the phenotypic heterogeneity of MCL and underscores the need for histopathologic correlation and, in some instances, ancillary genetic studies to accurately classify B-cell lymphomas.
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PMID:An unusual case of leukemic mantle cell lymphoma with a blastoid component showing loss of CD5 and aberrant expression of CD10. 1527 40

The immunohistochemical investigation used 55 primary hepatic tumors (hepatocellular carcinoma (HCC)--32, cholangiocellular carcinoma (CCC)--23). Wide panels of such antibodies as hepatocytic marker (Hep Par--1) CK-8, CK-19, polyclonal CEA, CD10, alpha-fetoprotein, TTF-1 as well as proliferative features of HCC (Ki-67) including regulators of stage-to-stage transition through mitoses of tumor cells (cyclin-D1 and A, genes p53 and RB), unrestricted tumor cell mitosis (telomerases), and intercellular adhesion marker (beta-catenin) were employed for differential diagnosis of neoplasia. The most efficient marker HCC was Hep Par--l (sensitivity--100%, specificity--92%) while the sensitivity of CCC (CK-19) was 83% and specificity--78%. Of particular importance for differentiation between HCC and CCC were the nature of microcirculatory flow identifiable with the aid of CD31 and presence of pseudocapsule in HCC detected by means of calponin. CEA and CD10 played a part too while the remaining markers were either expressed very seldom (alpha-fetoprotein) or absent (TTF-1). Most nuclear antigens (Ki-67, cyclin-A, p53 and RB) were intensely expressed in poorly-differentiated HCC cells. Cyclin-D1 and mutated suppressor-gene p53 expression involved lowered overall and relapse-free survival.
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PMID:[The significance of immunohistochemistry in the investigation of liver neoplasms: differential diagnosis, prognostic markers]. 1894 95


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