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The role of CD30 in the pathogenesis of haematopoietic malignancies

The role of CD30 in the pathogenesis of haematopoietic malignancies
The role of CD30 in the pathogenesis of haematopoietic malignancies
CD30, a member of the tumour necrosis factor receptor superfamily, is overexpressed by malignant cells of Hodgkin’s lymphoma and by anaplastic large cell lymphoma. CD30 overexpression has been attributed, at least in part, to constitutive expression of JunB, a transcription factor belonging to the AP-1 family that binds to the CD30 promoter. Overexpression of CD30 in Hodgkin’s lymphoma cells is thought to result in ligand-independent signaling, leading to activation of nuclear factor-?B and survival of the malignant cells. In anaplastic large cell lymphoma, CD30 triggering induces growth arrest and, under certain circumstances, cell death. Finally, transmembrane signalling by CD30 might be regulated by a soluble form of CD30 that is released by proteolytic cleavage of membrane-anchored CD30.
ALCL, anaplastic large cell lymphoma; CD30L, CD30 ligand; CD40L, CD40 ligand; CLL, chronic lymphocytic leukaemia; ERK, extracellular-regulated kinase; FasL, Fas ligand; HL, Hodgkin’s lymphoma; H-RS, Hodgkin and Reed-Sternberg; JNK, Jun N-terminal kinase; mAb, monoclonal antibody; MAPK, mitogen-activated protein kinase; MS, microsatellite sequence; NF-?B, nuclear factor-?B; TNF, tumour necrosis factor; TNFR, TNF receptor; TRAF, TNF receptor-associated factor
1471-4892
355-359
Al-Shamkhani, Aymen
0a40b3ce-9d71-4d41-9369-7212f0a84504
Al-Shamkhani, Aymen
0a40b3ce-9d71-4d41-9369-7212f0a84504

Al-Shamkhani, Aymen (2004) The role of CD30 in the pathogenesis of haematopoietic malignancies. Current Opinion in Pharmacology, 4 (4), 355-359. (doi:10.1016/j.coph.2004.02.007).

Record type: Article

Abstract

CD30, a member of the tumour necrosis factor receptor superfamily, is overexpressed by malignant cells of Hodgkin’s lymphoma and by anaplastic large cell lymphoma. CD30 overexpression has been attributed, at least in part, to constitutive expression of JunB, a transcription factor belonging to the AP-1 family that binds to the CD30 promoter. Overexpression of CD30 in Hodgkin’s lymphoma cells is thought to result in ligand-independent signaling, leading to activation of nuclear factor-?B and survival of the malignant cells. In anaplastic large cell lymphoma, CD30 triggering induces growth arrest and, under certain circumstances, cell death. Finally, transmembrane signalling by CD30 might be regulated by a soluble form of CD30 that is released by proteolytic cleavage of membrane-anchored CD30.
ALCL, anaplastic large cell lymphoma; CD30L, CD30 ligand; CD40L, CD40 ligand; CLL, chronic lymphocytic leukaemia; ERK, extracellular-regulated kinase; FasL, Fas ligand; HL, Hodgkin’s lymphoma; H-RS, Hodgkin and Reed-Sternberg; JNK, Jun N-terminal kinase; mAb, monoclonal antibody; MAPK, mitogen-activated protein kinase; MS, microsatellite sequence; NF-?B, nuclear factor-?B; TNF, tumour necrosis factor; TNFR, TNF receptor; TRAF, TNF receptor-associated factor

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Published date: 2004

Identifiers

Local EPrints ID: 26186
URI: https://eprints.soton.ac.uk/id/eprint/26186
ISSN: 1471-4892
PURE UUID: 21380c73-e6b8-4119-996c-8e6e5e6566b1
ORCID for Aymen Al-Shamkhani: ORCID iD orcid.org/0000-0003-0727-4189

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Date deposited: 20 Apr 2006
Last modified: 15 Aug 2019 00:50

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