Genes (34)
Species: human : 34 | |
Human | CYSLTR2 | 57105 | cysteinyl leukotriene receptor 2 | A G protein-coupled receptor (GPCR) is encoded within the genome of Kaposi;s sarcoma- associated herpesvirus (KSHV)/human herpesvirus 8, a virus that may be involved in the pathogenesis of Kaposi;s sarcoma and primary effusion lymphomas. | Human | PABPC1 | 26986 | poly(A) binding protein, cytoplasmic 1 | PABP interacts with HHV-8 K10/10.1 protein in infected primary effusion lymphoma (PEL) cell lines | Human | SAP30 | 8819 | Sin3A-associated protein, 30kDa | To better understand the contribution of LANA to tumorigenesis and to the PEL phenotype, we performed a yeast two-hybrid screen which identified the corepressor protein SAP30 as a LANA binding protein. | Human | TNFRSF10D | 8793 | tumor necrosis factor receptor superfamily, member 10d, decoy with truncated death domain | AZT and IFN-alpha mediated apoptosis in PEL was blocked by stable overexpression of dominant negative Fas Associated Death Domain (FADD), decoy receptor 2 (DcR2), soluble TRAIL receptor fusion proteins (DR-4 and DR-5) and thymidine. AZT and IFN-alpha mediated apoptosis in PEL was blocked by stable overexpression of dominant negative Fas Associated Death Domain (FADD), decoy receptor 2 (DcR2), soluble TRAIL receptor fusion proteins (DR-4 and DR-5) and thymidine. | Human | TCL1A | 8115 | T-cell leukemia/lymphoma 1A | Infection of HHV-8+ primary effusion lymphoma cells with a recombinant Epstein-Barr virus leads to restricted EBV latency, altered phenotype, and increased tumorigenicity without affecting TCL1 expression. Human herpesvirus-8 infected primary effusion lymphomas (PEL) and multiple myelomas are uniformly TCL1 negative, whereas all other transformed B cell lines tested express moderate to abundant TCL1. | Human | XBP1 | 7494 | X-box binding protein 1 | The unfolded protein response is partially activated in PEL, but is fully activated in plasma cell tumors, linking endoplasmic reticulum stress to plasma cell development through XBP-1. | Human | STAT3 | 6774 | signal transducer and activator of transcription 3 (acute-phase response factor) | Inhibition of STAT3 signaling induces apoptosis and decreases survivin expression in primary effusion lymphoma. findings suggest that activated STAT3 signaling directly contributes to malignant progression of primary effusion lymphoma by preventing apoptosis, acting through the prosurvival protein survivin | Human | SSTR1 | 6751 | somatostatin receptor 1 | To investigate whether HHV-8 may contribute to PEL development in the absence of EBV, the expression of seven potentially oncogenic HHV-8 open reading frames (ORFs) (ORF72/viral cyclin D, ORF16/viral bcl-2, ORF74/viral G-protein coupled receptor, ORFK2/viral IL-6, ORFK13/viral FLICE inhibitory protein, ORFK9/viral interferon regulatory factor, and ORFK1, equivalent to the gene encoding herpesvirus saimiri transforming protein) was assessed by reverse transcriptase-polymerase chain reaction (RT-PCR) in an EBV-negative PEL presenting in an HIV-negative patient. | Human | SPI1 | 6688 | spleen focus forming virus (SFFV) proviral integration oncogene | Ectopic expression of Oct-2 was able to fully restore PU.1 promoter activity in the PEL cell line BCBL-1, while PU.1 expression also reconstituted the activity of the lambdaB Ets-IRF site. | Human | SDC1 | 6382 | syndecan 1 | Using these mAbs, we have demonstrated that: (a) tumour cells from PEL expressed a syndecan-1 isoform with a higher molecular weight than that present on malignant plasma cells; (b) syndecan-1 expressed by PEL cells had a core protein identical in size to that expressed by plasma cells, suggesting that differences in syndecan-1 size were due to different GAG chains attached to an identical protein backbone; (c) the PEL-specific isoform of syndecan-1, which probably represented the major proteoglycan expressed by these cells, was effective in mediating cell adhesion to type I collagen substrates. High levels of a putatively syndecan-1 isoform have recently been found on neoplastic cells of primary effusion lymphoma (PEL). Immunophenotypic studies revealed that the lymphoma population expressed an antigenic profile consistent with PEL, i.e. the absence of common B- and T-cell markers (non-B, non-T phenotype) coupled to CD138 positivity. | Human | POU2F2 | 5452 | POU class 2 homeobox 2 | However, in PEL-derived B-cell lines, PU.1 expression was completely abrogated; expression of the B cell specific transcription factor Oct-2, which is known to regulate PU.1 expression, was also abolished. Ectopic expression of Oct-2 was able to fully restore PU.1 promoter activity in the PEL cell line BCBL-1, while PU.1 expression also reconstituted the activity of the lambdaB Ets-IRF site. | Human | POU2AF1 | 5450 | POU class 2 associating factor 1 | Silenced endogenous B cell genes representing a surface receptor, B29 (Igbeta, CD79b), a signaling molecule, TCL1, and a transcription factor, Bob1 (OCA-B, OBF-1), were reactivated by 5-aza-2;-deoxycytidine, indicating that gene silencing in HRS and PEL cells is due to DNA methylation. | Human | PNLIP | 5406 | pancreatic lipase | The nucleotides of the PL gene (pel) were sequenced. | Human | PAX5 | 5079 | paired box 5 | This case is the first report of an HHV8- PEL with t(9;14) involving a PAX-5 gene rearrangement in an HIV-seronegative patient. These findings suggest that there may be an additional subcategory of primary effusion lymphoma that is not associated with HHV8 nor c-MYC(R) but is pathogenetically associated with the PAX-5 gene or hepatitis C virus. At present, there is no case report of HHV8- primary effusion lymphoma (PEL) with t(9;14)(p13;q32) involving both PAX-5 and immunoglobulin heavy chain gene rearrangement, which is a rare translocation in B-cell non-Hodgkin;s lymphoma, in an HIV- patient. Herpes virus type 8-negative primary effusion lymphoma associated with PAX-5 gene rearrangement and hepatitis C virus: a case report and review of the literature. In addition, this PEL case harbored PAX-5 gene mutations, which have been recently demonstrated as a key feature of the proto-oncogene hypermutation process involved in the pathogenesis of some lymphoma types. | Human | OSM | 5008 | oncostatin M | In clonogenic assays, interferon-alpha (IFN-alpha) and IFN-gamma suppressed the clonal growth of the PEL cells, but GM-CSF, IL-4, IL-6, IL-8, IL-10, and oncostatin M did not change it. Using specific ELISAs, PEL cell lines were found to produce large amounts of interleukin-6 (IL-6; 10-5000 pg/ml), IL-6 soluble receptor (IL-6sR; 30-600 pg/ml), IL-10 (600-80,000 pg/ml) and oncostatin M (OSM; 50-80 pg/ml) which in most cases were significantly higher than the levels produced by the Burkitt, B-NHL or myeloma cell lines; on the contrary, PEL cell lines did not elaborate significant levels of macrophage inhibitory protein (MIP-1alpha) and leukemia inhibitory factor (LIF). Using specific ELISAs, PEL cell lines were found to produce large amounts of interleukin-6 (IL-6; 10-5000 pg/ml), IL-6 soluble receptor (IL-6sR; 30-600 pg/ml), IL-10 (600-80,000 pg/ml) and oncostatin M (OSM; 50-80 pg/ml) which in most cases were significantly higher than the levels produced by the Burkitt, B-NHL or myeloma cell lines; on the contrary, PEL cell lines did not elaborate significant levels of macrophage inhibitory protein (MIP-1alpha) and leukemia inhibitory factor (LIF). In summary, PEL cell lines produce high amounts of cytokines (IL-6, IL-10, OSM); proliferation could be inhibited by blocking the receptors of the IL-6 signaling pathway. In clonogenic assays, interferon-alpha (IFN-alpha) and IFN-gamma suppressed the clonal growth of the PEL cells, but GM-CSF, IL-4, IL-6, IL-8, IL-10, and oncostatin M did not change it. Some PEL cases also release oncostatin M. PEL cell lines did not respond proliferatively to IL-6, IL-10, IL-11, LIF, MIP-1alpha, or OSM. Some PEL cases also release oncostatin M. | Human | NOTCH1 | 4851 | notch 1 | In this report, we show that the activated intracellular domain of Notch1 (ICN) is aberrantly accumulated in KSHV latently infected pleural effusion lymphoma (PEL) cells. | Human | MYC | 4609 | v-myc avian myelocytomatosis viral oncogene homolog | These findings indicate that vIRF-3 can effectively stimulate c-Myc function in primary effusion lymphoma cells and consequently contribute to de-regulation of B-cell growth and differentiation | Human | MNDA | 4332 | myeloid cell nuclear differentiation antigen | MNDA transcript was undetectable in three PEL cell lines by reverse-transcription polymerase chain reaction, but it was induced by interferon alpha (IFNalpha). Moreover, LANA and MNDA were co-localized in the nuclei of MNDA-expressing PEL cells. | Human | LTA4H | 4048 | leukotriene A4 hydrolase | Leukotriene A4 Hydrolase Expression in PEL Cells Is Regulated at the Transcriptional Level and Leads to Increased Leukotriene B4 Production. Among these, four genes involved in cell migration and chemotaxis were strongly up-regulated in PEL cells: leukotriene A4 (LTA4) hydrolase (LTA4H), IL-16, thrombospondin-1 (TSP-1), and selectin-P ligand (PSGL-1). | Human | KRT13 | 3860 | keratin 13 | We have previously examined the transcription and splicing of open reading frames (ORFS) 71 (K13), 72, and 73 of Kaposi;s sarcoma-associated herpesvirus (KSHV) in the primary effusion lymphoma cell line BCP-1 (latently infected with KSHV) (45). | Human | JUN | 3725 | jun proto-oncogene | Gene silencing experiments by RNA interference demonstrate that vFLIP in BCBL-1 endogenously infected primary effusion lymphoma (PEL) cells mediates JNK/AP1 activation and cIL-6 expression. | Human | IRF7 | 3665 | interferon regulatory factor 7 | Western immunoblot and immunohistochemical analyses confirmed that the cellular IRF7 protein levels were strongly upregulated during the early lytic cycle both in KSHV-infected DMVEC and in the body cavity-based lymphoma BCBL1 PEL cell line. | Human | IKBKB | 3551 | inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase beta | In the HHV-8-positive PEL cell line BCBL-1, tetradecanoyl phorbol acetate (TPA) induction of the lytic cycle activates the NF-kappaB pathway, and this activation requires the induction of the IKKbeta component of the classical IkappaB kinase (IKK) complex. | Human | IGHM | 3507 | immunoglobulin heavy constant mu | In contrast, the VH gene segment expressed by tumor cells of the BC-3 cell line, which was originated from an EBV-negative PEL obtained from an HIV-negative patient, was unmutated, suggesting a pre-germinal center B cell origin for tumor cells of this particular PEL cell line. | Human | GSK3B | 2932 | glycogen synthase kinase 3 beta | manipulation of GSK-3beta activity may be a mechanism by which HHV-8 latency-associated nuclear antigen (LANA) may modify transcriptional activity and contribute to the phenotype of HHV-8 primary effusion lymphoma |
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