Differential Expression of BCL-6, Cd 138/Syndecan-1 and Ebv-Encoded Latent Membrane Protein-1 Identifies Distinct Histogenetic Subsets of Aids-Related Non-Hodgkin's Lymphomas.

Carbone, Antonino; Gaïdano, Gianluca; Gloghini, Annunziata; Larocca, Luigi Maria; Capello, Daniela; Tirelli, Umberto; Falini, Brunangelo; Dalla‐Favera, Riccardo

doi:10.1097/00042560-199804010-00117

Cited by 57 publications

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“…Under the study conditions we describe, CD138 and VS38 were more effective and specific in detecting plasmacytic differentiation in tissue microarrays as well as in individually tested cases of LPL and MZL. Our findings of the immunoreactivity of CD138 and VS38 in LPL and MZL with and without plasmacytic differentiation are entirely in agreement with previous studies for these markers (24,25,27,28,(45)(46)(47)(48). Although careful morphologic correlation of consecutive sections in cases immunoreactive for all three markers revealed similar patterns of distribution of stained cells, MUM1 consistently stained a larger number of lesional cells than did CD138 or VS38.…”

Section: Figuresupporting

confidence: 93%

“…Two such markers, CD138 and VS38, are currently used in paraffin sections. CD138, a member of the syndecan family of integral membrane proteoglycans, is thought to orchestrate cytoadhesive signaling and plays a role in the pathogenesis of multiple myeloma and in the detection of plasmacytic differentiation (17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30). VS38 recognizes a transmembrane protein, p63, which resides in the rough endoplasmic reticulum and mediates increased secretory function (31)(32)(33).…”

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confidence: 99%

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Analysis of MUM1/IRF4 Protein Expression Using Tissue Microarrays and Immunohistochemistry

et al. 2001

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The gene encoding MUM1 was characterized as a possible translocation partner in chromosomal abnormalities involving a significant number of multiple myelomas. The overexpression of the MUM1 protein as a result of translocation t(6;14) (p25;q32) identified MUM1 as a putative regulatory molecule involved in B-cell differentiation and tumorigenesis. The expression of MUM1 protein in multiple myelomas supports this hypothesis. In the current study, using tissue microarray technology, we have tested the expression of the MUM1 protein in 1335 human malignancies and normal tissues. Our data show that the MUM1 protein is expressed in a wide spectrum of hematolymphoid neoplasms and in malignant melanomas but is absent in other human tumors. In addition, in tissue microarrays as well as in conventional paraffin sections, MUM1 staining was found to lack specificity in detecting plasmacytic differentiation as compared with two markers, CD138/Syndecan and VS38, commonly used in paraffin immunohistochemistry for detection of plasma cells.

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Section: Figuresupporting

confidence: 93%

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confidence: 99%

Analysis of MUM1/IRF4 Protein Expression Using Tissue Microarrays and Immunohistochemistry

et al. 2001

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“…Conversely, mutations of the 5Ј noncoding regions of BCL-6 have been recently suggested to associate with a significant fraction of PEL. 2 PEL occurs predominantly, but not exclusively among HIVinfected patients representing about 3% of all AIDS-NHLs, but less than 0.5% of all non-AIDS-high grade NHLs. 1,3 The clinical outcome of AIDS-PEL is very poor as median survival ranged from 2 to 6 months; most patients have advanced AIDS and are poor candidates for aggressive chemotherapy.…”

Section: Body Cavity-based Lymphoma -Primary Effusion Lymphomamentioning

confidence: 98%

“…AIDS-NHL represents a pathologically very heterogenous group of lymphomas ranging from small non-cleaved cell lymphoma to diffuse large cell lymphoma; the latter group includes large non-cleaved cell lymphoma and large cell immunoblastic lymphoma plasmacytoid. 2 Serous effusions are a common complication of lymphomas, mostly as secondary lymphomatous effusions originating from clinically evident solid NHL. Recently, a unique type of primary lymphomatous effusion has been recognized in AIDS patients.…”

Section: Body Cavity-based Lymphoma -Primary Effusion Lymphomamentioning

confidence: 99%

“…These lymphoma cells grow exclusively or mainly in pleural, pericardial, or peritoneal cavities as lymphomatous effusions ('liquid lymphomas'), usually without an identifiable tumor mass or lymphoadenopathy throughout their clinical course. 5,6 The PEL cells have indeterminate immunophenotypes but B cell genotypes with clonal rearrangements of the immunoglobulin genes; positivity for CD138 suggests a mature, preterminal or terminal plasma cell stage of B cell differentiation 2,5,7 (Figure 1). The neoplastic cells consistently lack most of the genetic lesions commonly seen in mature B cell malignancies, eg rearrangements of MYC, BCL-2 and BCL-6 as well as mutations of p53.…”

Section: Body Cavity-based Lymphoma -Primary Effusion Lymphomamentioning

confidence: 99%

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Lymphoma cell lines: in vitro models for the study of HHV-8+ primary effusion lymphomas (body cavity-based lymphomas)

Drexler

Uphoff

Gaïdano³

et al. 1998

Leukemia

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Syndecan-1 expression is up-regulated in pancreatic but not in other gastrointestinal cancers

et al. 2000

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Syndecan‐1 belongs to the syndecan family of cell surface transmembrane heparan‐sulfate proteoglycans, which participate in cell proliferation, cell migration and cell‐matrix interactions. Decreased expression of syndecan‐1 has been observed in some gastrointestinal malignancies, and it is thought that high levels of syndecan‐1 correlate with the maintenance of epithelial morphology and inhibition of invasiveness. In our study, we characterized the expression of syndecan‐1 in normal, chronic pancreatitis and primary and metastatic human pancreatic cancer tissues, in cultured pancreatic cancer cell lines and in esophageal, gastric, colon, and liver cancers. Pancreatic cancer cell lines expressed syndecan‐1 mRNA and protein at variable levels. In addition, these cells also released syndecan‐1 into the culture medium. Pancreatic cancer tissues markedly over‐expressed syndecan‐1 mRNA in comparison with both chronic pancreatitis (2.4‐fold increase, p < 0.01) and normal pancreatic samples (10.6‐fold increase, p < 0.01). There was no difference in syndecan‐1 mRNA expression between early and advanced tumors. By in situ hybridization and immunohistochemistry, syndecan‐1 expression was evident at relatively low levels in the ductal cells and less frequently in acinar cells of the normal pancreas. In chronic pancreatitis, syndecan‐1 was present at low to moderate levels in areas with atrophic acinar cells and ductular complexes. In contrast, in pancreatic cancer tissues, syndecan‐1 was present at moderate to high levels in the majority of the cancer cells within the tumor mass and also in metastatic lesions of pancreatic tumors. Syndecan‐1 mRNA levels in other gastrointestinal malignancies (esophageal, gastric, colon and liver cancers) were not significantly different from the levels observed in the corresponding normal samples. Together, our findings suggest that syndecan‐1 expression by pancreatic cancer cells may be of importance in the pathobiology of this disorder and that its role in pancreatic cancer seems to be different from that in other gastrointestinal malignancies. Int. J. Cancer 88:12–20, 2000. © 2000 Wiley‐Liss, Inc.

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Differential Expression of BCL-6, Cd 138/Syndecan-1 and Ebv-Encoded Latent Membrane Protein-1 Identifies Distinct Histogenetic Subsets of Aids-Related Non-Hodgkin's Lymphomas.

Cited by 57 publications

References 0 publications

Analysis of MUM1/IRF4 Protein Expression Using Tissue Microarrays and Immunohistochemistry

Analysis of MUM1/IRF4 Protein Expression Using Tissue Microarrays and Immunohistochemistry

Lymphoma cell lines: in vitro models for the study of HHV-8+ primary effusion lymphomas (body cavity-based lymphomas)

Syndecan-1 expression is up-regulated in pancreatic but not in other gastrointestinal cancers

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