Analysis of CARMA1/BCL10/MALT1 expression in Reed – Sternberg cells of classical Hodgkin lymphoma

Ré, Daniel; Hartlapp, Ingo; Greiner, Axel; Diehl, Volker; Wickenhauser, Claudia

doi:10.1080/10428190701784722

Cited by 4 publications

(3 citation statements)

References 10 publications

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“…[28][29][30] However, the function of LMP2A in enhancing NF-kB signaling in Hodgkin's lymphoma is less clear, because HRS cells have largely lost their B-cell phenotype concomitant with the downregulation of many BCR signaling adaptors. [31][32][33] Nevertheless, LMP2A-triggered NF-kB activation may be involved in preventing apoptosis in the initial phase of Hodgkin's lymphoma pathogenesis.…”

Section: Control Of Nf-jb By Cell-intrinsic and Extrinsic Mechanisms mentioning

confidence: 99%

Mechanisms and consequences of constitutive NF-κB activation in B-cell lymphoid malignancies

et al. 2014

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The discovery of constitutive nuclear factor-κB (NF-κB) activation in Hodgkin's lymphoma tumor cells almost two decades ago was one of the first reports that directly connected deregulated NF-κB signaling to human cancer. Subsequent studies demonstrated that enhanced NF-κB signaling is a common hallmark of many lymphoid malignancies, including Hodgkin lymphoma, mucosa-associated lymphoid tissue lymphoma, diffuse large B-cell lymphoma and multiple myeloma. By inducing an anti-apoptotic and pro-proliferative gene program, NF-κB is involved in lymphoma survival and growth. Identification of somatic mutations that led to activation of oncogenes and inactivation of tumor suppressor genes in the pathway revealed that specific pathogenic mechanisms are responsible for constitutive NF-κB activation in different lymphoma entities. Thus, the identification of distinct oncogenic events is reflecting the diverse cellular origins of the different lymphomas. Further, elucidation of the mechanisms that drive NF-κB in lymphoma is of high clinical relevance as it will allow the design of target-directed precision therapy. Indeed, a number of drugs that impair constitutive NF-κB activation in lymphoid malignancies are currently in preclinical or clinical development.

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Section: Control Of Nf-jb By Cell-intrinsic and Extrinsic Mechanisms mentioning

confidence: 99%

Mechanisms and consequences of constitutive NF-κB activation in B-cell lymphoid malignancies

et al. 2014

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“…Perhaps, the high prevalence of NFkB abnormalities in HL is able to compensate for survival mechanisms mediated in the absence of a BCR. In any case, in HL [40] and other B cell tumors several kinds of abnormalities have been found in the protein complex that transduces NFkB activating signals from the BCR. MALT1 was initially identified as an oncogenic protein commonly expressed in a subset of MALT.L.…”

Section: Introductionmentioning

confidence: 99%

A critical role for the NFkB pathway in multiple myeloma

2010

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NFkB transcription factors play a key role in the survival and proliferation of many kinds of B-cell tumors, including multiple myeloma (MM). It was shown that NFkB activation in MM tumors results mainly from extrinsic signaling by APRIL and BAFF ligands that stimulate receptors on normal plasma cells as well as on pre-malignant monoclonal gammopathy of undetermined significance (MGUS) and MM tumors. However, the mutations that occur during MM progression and that constitutively activate NFkB would be expected to decrease dependence of tumor cells on the bone marrow microenvironment. These mutations can activate the classical or alternative NFkB pathways selectively, but usually both pathways are activated in MM. Significantly, activation of either NFkB pathway leads to a similar response of MM cell lines. This frequent activation of the alternative pathway distinguishes MM from other B-cell tumors, which more frequently have mutations that are predicted to activate only the classical NFkB pathway. Given the strong dependence of MGUS and MM tumors on NFkB pathway activation, inhibition by a combination of targeting extrinsic signaling plus both NFkB pathways appears to be an attractive therapeutic approach in MM tumors.

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“…Ähnlich häufig wird eine Proteinexpression für DLBCL (65% vs. 66%) und gastrale MZL (60% vs. 70%) beschrieben (Nakamura et al 2005;Zhao et al 2016). Für das HL konnte in einer vergleichbaren IHC-Analyse keine Proteinexpression nachgewiesen werden (Re et al 2008). Zwar sind auch HRS-Zellen auf ein starkes NFκB-Signaling angewiesen, jedoch erfolgt die NFκB-Aktivierung bei fehlendem BCR sowie der Herunterregulierung B-Zell-spezifischer Gene über alternative Signalwege (Bräuninger et al 2006;Jost et al 2007;Schwering et al 2003).…”

Section: Bcl11aunclassified

Vergleichende immunhistochemische Analyse onkogener Signalwegssignaturen in Lymphomen

Stauder¹

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Analysis of CARMA1/BCL10/MALT1 expression in Reed – Sternberg cells of classical Hodgkin lymphoma

Cited by 4 publications

References 10 publications

Mechanisms and consequences of constitutive NF-κB activation in B-cell lymphoid malignancies

Mechanisms and consequences of constitutive NF-κB activation in B-cell lymphoid malignancies

A critical role for the NFkB pathway in multiple myeloma

Vergleichende immunhistochemische Analyse onkogener Signalwegssignaturen in Lymphomen

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