Genes (86)
Species: human : 86 | |
Human | RNF213 | 57674 | ring finger protein 213 | KIAA1618 (ALO17) ia a novel fusion partner of anaplastic lymphoma kinase in anaplastic large-cell lymphoma and inflammatory myofibroblastic tumor cases | Human | LEF1 | 51176 | lymphoid enhancer-binding factor 1 | Surprisingly, none of the 21 cases of Th2-like PTCL studied, all cases of anaplastic large cell lymphoma, were immunoreactive for LEF-1 or TCF-1 (P < 0.0001), suggesting that LEF-1 and TCF-1 transcription factor expression may be lost in Th2 T cells or Th2-like PTCL. | Human | PTPN22 | 26191 | protein tyrosine phosphatase, non-receptor type 22 (lymphoid) | The authors studied expression of BLA.36 in 22 cases of ALCL, 13 cases of LyP, and 15 cases of HD. | Human | SWAP70 | 23075 | SWAP switching B-cell complex 70kDa subunit | All 4 T-cell lymphomas were nonreactive for SWAP-70: 0 of 3 peripheral T-cell lymphomas and 0 of 1 anaplastic large cell lymphoma. | Human | COPS5 | 10987 | COP9 signalosome subunit 5 | Using a 10% cutoff, p27 was positive in 12 of 66 (18.2%) ALCL tumors (5 ALK positive and 7 ALK negative), whereas JAB1 was detected in 47 of 53 (88.7%) tumors (15 ALK positive and 32 ALK negative) assessed. We assessed p27 and JAB1 in systemic anaplastic large cell lymphoma (ALCL), a group of tumors in which a substantial subset overexpresses anaplastic lymphoma kinase (ALK). CONCLUSIONS: p27 is absent or expressed at low levels in most ALCL tumors and inversely correlates with JAB1. | Human | MALT1 | 10892 | mucosa associated lymphoid tissue lymphoma translocation gene 1 | The disease entities are primarily exemplified by mantle cell lymphoma (the relative incidence, 3%, related with an aberrant expression of cyclin D1 activated by t(11;14) chromosomal translocation), follicular lymphoma (7%, with BCL2 by t(14;18) translocation), marginal zone B-cell lymphoma of MALT type (8%, with MALT1 by t(11;18) or t(14;18) translocation), adult T-cell leukemia/lymphoma (7%, but 20% in Kyushu, with human T-cell leukemia virus type 1 [HTLV1]), extranodal NK/T-cell lymphoma of nasal type (2%, with Epstein-Barr virus [EBV]), and anaplastic large cell lymphoma (2%, with ALK by t(2;5) translocation). | Human | TFG | 10342 | TRK-fused gene | TRK-fused gene (TFG) is a new partner of ALK in anaplastic large cell lymphoma producing two structurally different TFG-ALK translocations. Here we have identified TRK-fused gene (TFG) as a new ALK partner in 2 ALCL, 1 of which exhibited a t(2;3)(p23;q21). ALK expression has been instrumental in defining a homogeneous subset from the category of anaplastic large cell lymphoma, characterised by occurrence in young patients, primary systemic presentation, favorable prognosis, a broad morphological spectrum, nuclear and/or cytoplasmic immunostaining for ALK protein, and a number of possible fusion partner genes such as NPM, ATIC, TFG, TPM3 and CLTCL. In anaplastic large cell lymphoma, the ALK gene at 2p23 is known to be fused to NPM, TPM3, TPM4, TFG, ATIC, CLTC, MSN, and ALO17. These findings indicate that TFG can provide an alternative to NPM as a fusion partner responsible for activation of the ALK and the pathogenesis of ALCL. | Human | SOCS3 | 9021 | suppressor of cytokine signaling 3 | As SOCS3 is induced by activated signal transducer and activator of transcription 3 (STAT3), and ALK activates STAT3, we hypothesized that SOCS3 may play a role in ALK+ ALCL pathogenesis via the Janus kinase 3 (JAK3)-STAT3 pathway. These results show that SOCS3 is overexpressed in ALCL, attributable to JAK3-STAT3 activation and likely related to ALK in ALK+ tumors. overexpression of suppressor of cytokine signaling 3 is associated with anaplastic large cell lymphoma Suppressor of cytokine signaling 3 expression in anaplastic large cell lymphoma. In ALCL tumors that were assessed by immunohistochemistry, nine of 12 (75%) ALK+ tumors were SOCS3 positive and eight (67%) coexpressed pSTAT3. Using ALCL cell lines, we show by coimmunoprecipitation experiments that SOCS3 physically binds with JAK3 in vitro, and that JAK3 inhibition by WHI-P154 downregulates SOCS3 expression. Using a cDNA microarray, we found that suppressor of cytokine signaling 3 (SOCS3) is highly expressed in anaplastic lymphoma kinase (ALK)+ anaplastic large cell lymphoma (ALCL) cell lines. | Human | NR0B2 | 8431 | nuclear receptor subfamily 0, group B, member 2 | Loss of SHP1 enhances JAK3/STAT3 signaling and decreases proteosome degradation of JAK3 and NPM-ALK in ALK+ anaplastic large-cell lymphoma | Human | TCL1A | 8115 | T-cell leukemia/lymphoma 1A | Conversely, TCL1 was not expressed in Hodgkin/Reed-Sternberg cells, multiple myelomas, marginal zone B-cell lymphomas, CD30+ anaplastic large cell lymphoma, lymphoblastic T-cell lymphoma, peripheral T-cell lymphoma, and mycosis fungoides. | Human | CXCR4 | 7852 | chemokine (C-X-C motif) receptor 4 | Anaplastic large cell lymphoma, which typically expresses markers of Th2 differentiation, was immunoreactive for CXCR4/CD184 in 22 (88%) of 25 cases. | Human | TNFRSF4 | 7293 | tumor necrosis factor receptor superfamily, member 4 | In ALCL, all cases were immunonegative for OX40/CD134, and only a few cases (24%) were immunoreactive for CXCR3, whereas almost all cases (94%) were positive for ST2(L). CD134/OX40 expression is characteristic of certain entities (angioimmunoblastic lymphoma, angiocentric T-NHL) and a subset of T-NHLs of unspecified type, whereas CD30 expression is characteristic of ALCL and a largely non-overlapping subset of T-NHLs of unspecified type. | Human | TRAF2 | 7186 | TNF receptor-associated factor 2 | Activation of CD30 led to the induction of apoptotic death of ALCL cells, along with the selective reduction of TNF receptor-associated factor 2 and impairment in the ability of these cells to activate the pro-survival transcription factor nuclear factor kappa B (NF-kappa B). | Human | TRAF1 | 7185 | TNF receptor-associated factor 1 | Differential expression and function of A20 and TRAF1 in Hodgkin lymphoma and anaplastic large cell lymphoma and their induction by CD30 stimulation. Four of seven anaplastic large cell lymphomas weakly expressed TRAF1. Differential expression and function of A20 and TRAF1 in Hodgkin lymphoma and anaplastic large cell lymphoma and their induction by CD30 stimulation. In contrast, strong TRAF1 staining was present in only 1 of 17 cases of anaplastic large cell lymphoma, 0 of 15 cases of lymphocyte predominant Hodgkin lymphoma, and 2 of 36 cases of nonmediastinal diffuse large B-cell lymphoma. In contrast, strong TRAF1 staining was present in only 1 of 17 cases of anaplastic large cell lymphoma, 0 of 15 cases of lymphocyte predominant Hodgkin lymphoma, and 2 of 36 cases of nonmediastinal diffuse large B-cell lymphoma. We demonstrate that the expression of TRAF1 and activated c-Rel, two proteins that function in signaling events downstream of activated CD30 in Reed-Sternberg cells, reliably distinguish classical Hodgkin lymphoma from anaplastic large cell lymphoma, nodular lymphocyte predominant Hodgkin lymphoma, and nonmediastinal diffuse large B-cell lymphoma. We demonstrate that the expression of TRAF1 and activated c-Rel, two proteins that function in signaling events downstream of activated CD30 in Reed-Sternberg cells, reliably distinguish classical Hodgkin lymphoma from anaplastic large cell lymphoma, nodular lymphocyte predominant Hodgkin lymphoma, and nonmediastinal diffuse large B-cell lymphoma. Four of seven anaplastic large cell lymphomas weakly expressed TRAF1. | Human | TPM4 | 7171 | tropomyosin 4 | In anaplastic large cell lymphoma, the ALK gene at 2p23 is known to be fused to NPM, TPM3, TPM4, TFG, ATIC, CLTC, MSN, and ALO17. | Human | TIMP1 | 7076 | TIMP metallopeptidase inhibitor 1 | MATERIALS AND METHODS: We investigated 60 cases of Hodgkins lymphoma and anaplastic large cell lymphoma for TIMP-1 and EMMPRIN expression using immunohistochemistry. Thus, we tested the hypothesis that TIMP1 expression is related to STAT3 activation in lymphomas, with a focus on anaplastic large cell lymphomas (ALCLs), which are known to express high levels of phosphorylated/active STAT3 (pSTAT3). We speculate that EMMPRIN and TIMP-1 may be important in the pathogenesis of anaplastic large cell lymphoma and Hodgkins disease. EMMPRIN and TIMP-1 were co-expressed in two-thirds of the Hodgkins lymphomas and anaplastic large cell lymphomas. STAT3 directly contributes to the high level of TIMP1 expression in anaplastic lymphoma kinase-positive anaplastic large cell lymphoma | Human | TIA1 | 7072 | TIA1 cytotoxic granule-associated RNA binding protein | Cytotoxic molecule (CM) expression, specifically TIA1 and granzyme B, is predictive of prognosis in Hodgkin's-like anaplastic large cell lymphoma | Human | TCF7 | 6932 | transcription factor 7 (T-cell specific, HMG-box) | Surprisingly, none of the 21 cases of Th2-like PTCL studied, all cases of anaplastic large cell lymphoma, were immunoreactive for LEF-1 or TCF-1 (P < 0.0001), suggesting that LEF-1 and TCF-1 transcription factor expression may be lost in Th2 T cells or Th2-like PTCL. | Human | STAT5A | 6776 | signal transducer and activator of transcription 5A | Acts as a key tumor suppressor by reciprocally inhibiting expression of oncogenic nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK) in T-cell anaplastic large cell lymphomas | Human | STAT3 | 6774 | signal transducer and activator of transcription 3 (acute-phase response factor) | In this study, we evaluated comprehensively STAT3 activation status in anaplastic large cell lymphoma (ALCL) cell lines and pretreatment ALCL tumors. Thus, we tested the hypothesis that TIMP1 expression is related to STAT3 activation in lymphomas, with a focus on anaplastic large cell lymphomas (ALCLs), which are known to express high levels of phosphorylated/active STAT3 (pSTAT3). Differential expression and clinical significance of tyrosine-phosphorylated STAT3 in ALK+ and ALK- anaplastic large cell lymphoma. The physiological role of Stat3 in anaplastic large cell lymphomas and the effects of inhibition of expression of the gene on tumorigenesis is reported | Human | SPN | 6693 | sialophorin | Immunohistochemical staining established the T-cell origin of the neoplasm with strong expression of CD45, CD3, CD43, and CD2 and also showed expression of CD30 consistent with the histologic features that suggested ALCL. MT1 (CD43), UCHL-1 (CD45RO), and P80 were totally negative in the six patients and in Hodgkin disease, whereas they were expressed variably in ALCL. Paraffin-embedded, formalin-fixed tissue sections from 25 cases of CD30-positive LPDs (10 noncutaneous ALCL, 15 PC CD30-positive LPDs) were immunostained for CD3, CD20 (L26), CD43 (Leu22), CD30 (BerH2), anaplastic lymphoma kinase (ALK-1), CD95, and CD95L (C-33). Examination of the pleural fluid revealed ALCL positive for Ki-1 (CD30), LCA (CD45), UCHL-1 (CD45RO), CD43, CD3, and epithelial membrane antigen. No expression of anaplastic large cell lymphoma kinase (ALK), CD10, CD23, CD30, CD43, bcl-6, cyclin D1, p53 or p16(INK4a) could be seen. We conclude that the immunophenotypic profile of the anaplastic cells in IMFH (lack of CD15, CD30, CD43, CD45/CD45RB, CD45RO, CD20) differs from most cases of Hodgkin;s disease (ICD30+, CD15+/-) and from Ki-1 anaplastic large cell lymphoma (CD30+, CD45/CD45RB+/-, CD43+/-, CD45RO+/-, CD20-/+). | Human | S100A9 | 6280 | S100 calcium binding protein A9 | The discrepancy among KP1, MAC387 and LN-5 reactivities may represent the concurrent occurrence of ALCL and lymphomatoid papulosis. | Human | CLIP1 | 6249 | CAP-GLY domain containing linker protein 1 | A novel 160-kDa intermediate filament associated protein, named restin (Reed-Sternberg intermediate filament associated protein), is specifically expressed in the malignant cells of Hodgkin;s disease and anaplastic large cell lymphoma (Ki-1 lymphoma). As expected, Restin was also expressed in Hodgkin cell lines L428, L428KSA, Co, and KM-H2 and the anaplastic large-cell lymphoma cell line Karpas 299, which was confirmed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting, as well as Northern blotting. Hence, restin may contribute to neoplastic transformation in Hodgkin;s disease and anaplastic large cell lymphoma. The presence of Restin in both Hodgkin;s disease and anaplastic large-cell lymphoma is intriguing and might indicate a role of this structural protein in the pathogenesis of both conditions. Expression of the novel intermediate filament-associated protein restin in Hodgkin;s disease and anaplastic large-cell lymphoma. Restin in Hodgkin;s disease and anaplastic large cell lymphoma. Study of the mechanisms leading to restin overexpression may provide important data on the etiology of Hodgkin;s disease and its relation to anaplastic large cell lymphoma. Restin was also highly expressed in anaplastic large-cell lymphoma (so-called Ki-1 lymphoma). | Human | REL | 5966 | v-rel avian reticuloendotheliosis viral oncogene homolog | Nuclear staining for c-Rel, a pattern consistent with NFkappaB activation, was observed in the Reed-Sternberg cells in 23 of 25 cases of classical Hodgkin lymphoma but only in 1 of 15 cases of anaplastic large cell lymphoma and 3 of 15 cases of nodular lymphocyte predominant Hodgkin lymphoma. We demonstrate that the expression of TRAF1 and activated c-Rel, two proteins that function in signaling events downstream of activated CD30 in Reed-Sternberg cells, reliably distinguish classical Hodgkin lymphoma from anaplastic large cell lymphoma, nodular lymphocyte predominant Hodgkin lymphoma, and nonmediastinal diffuse large B-cell lymphoma. | Human | RB1 | 5925 | retinoblastoma 1 | Rb is absent or phosphorylated in most anaplastic large cell lymphoma cell lines and tumors and absence of Rb expression is associated with better clinical outcome in patients with ALCL |
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