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The role of AP-1 and epigenetics in ALCL
- Source :
- Frontiers in Bioscience. 7:226-235
- Publication Year :
- 2015
- Publisher :
- IMR Press, 2015.
-
Abstract
- Anaplastic large cell lymphoma (ALCL) is an aggressive, highly proliferative, T-cell lymphoma with increasing incidence worldwide. Anaplastic Lymphoma Kinase (ALK) fusions occur in about 50% of all cases. Most ALK positive cases of ALCL harbor the t(2;5) translocation that leads to expression of Nucleophosmin-Anaplastic Lymphoma Kinase (NPM-ALK). NPM-ALK induces a variety of oncogenic signaling pathways that lead to malignant transformation of T-cells via Activator Protein-1 (AP-1), STAT3 and other (transcription) factors. In addition to the commonly known AP-1 activators Mitogen-Activated Protein Kinases (MAPKs), there are other signaling pathways, such as PI3K/mTOR/AKT, which are implicated in AP-1 activation/expression in ALCL. The AP-1 factor JUNB was shown to drive ALCL proliferation and the expression of the characteristic ALCL Ki-1 antigen, CD30. cJUN and JUNB target PDGFRB, thereby leading to tumor progression and dissemination. Furthermore, aberrant gene expression in ALCL is frequently accompanied by changes in epigenetic regulatory mechanisms, such as DNA methylation patterns. Here, we discuss the role of AP-1 in the pathogenesis of ALCL and provide an overview of pathological epigenetic changes in ALCL cells.
- Subjects :
- General Immunology and Microbiology
CD30
JUNB
PDGFRB
Biology
medicine.disease
General Biochemistry, Genetics and Molecular Biology
Epigenesis, Genetic
Transcription Factor AP-1
Tumor progression
hemic and lymphatic diseases
medicine
Cancer research
Animals
Humans
Lymphoma, Large-Cell, Anaplastic
Anaplastic lymphoma kinase
Anaplastic large-cell lymphoma
Protein kinase B
PI3K/AKT/mTOR pathway
Subjects
Details
- ISSN :
- 19450524 and 19450516
- Volume :
- 7
- Database :
- OpenAIRE
- Journal :
- Frontiers in Bioscience
- Accession number :
- edsair.doi.dedup.....066cf03fb4a216bf2330358224ad189f