Abstract
Classical Hodgkin lymphoma (cHL) is now recognized as a B-cell-derived lymphoma which is characterized by only about 1% malignant pathognomonic Hodgkin and Reed-Sternberg (HRS) cells and an abundant infiltrate of reactive bystander cells. HRS cells are unique with respect to their lost B-cell-specific gene expression pattern and recurrent genetic lesions. Aberrant activity of Notch signaling, a highly conserved developmental pathway, acts as a negative regulator of the B cell program in HRS cells and thereby contributes to their reprogramming. Another striking feature and the major pathogenetic mechanism in HRS cells is constitutive NF-κB activation. A number of aberrations that contribute to canonical NF-κB activity in HRS cells have been described such as genetic lesions, deregulated receptor signaling and Epstein-Barr virus (EBV) infection. The importance of Notch and NF-κB signaling for cHL pathogenesis, their potential cross-talk and implications for future therapeutic applications are being discussed.
Keywords: Notch, NF-κB, Hodgkin lymphoma, B cell lymphoma, Hodgkin/Reed-Sternberg cells, gene transcription, mutations, immunoprecipitation, inflammatory cells, cytokine, helix-loop-helix proteins, Epstein-Barr virus, Multiple Myeloma, B-chronic lymphocytic leukemia, tumor suppressor gene
Current Molecular Medicine
Title: Notch and NF-κB Signaling Pathways in the Biology of Classical Hodgkin Lymphoma
Volume: 11 Issue: 3
Author(s): R. Schwarzer and F. Jundt
Affiliation:
Keywords: Notch, NF-κB, Hodgkin lymphoma, B cell lymphoma, Hodgkin/Reed-Sternberg cells, gene transcription, mutations, immunoprecipitation, inflammatory cells, cytokine, helix-loop-helix proteins, Epstein-Barr virus, Multiple Myeloma, B-chronic lymphocytic leukemia, tumor suppressor gene
Abstract: Classical Hodgkin lymphoma (cHL) is now recognized as a B-cell-derived lymphoma which is characterized by only about 1% malignant pathognomonic Hodgkin and Reed-Sternberg (HRS) cells and an abundant infiltrate of reactive bystander cells. HRS cells are unique with respect to their lost B-cell-specific gene expression pattern and recurrent genetic lesions. Aberrant activity of Notch signaling, a highly conserved developmental pathway, acts as a negative regulator of the B cell program in HRS cells and thereby contributes to their reprogramming. Another striking feature and the major pathogenetic mechanism in HRS cells is constitutive NF-κB activation. A number of aberrations that contribute to canonical NF-κB activity in HRS cells have been described such as genetic lesions, deregulated receptor signaling and Epstein-Barr virus (EBV) infection. The importance of Notch and NF-κB signaling for cHL pathogenesis, their potential cross-talk and implications for future therapeutic applications are being discussed.
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Cite this article as:
Schwarzer R. and Jundt F., Notch and NF-κB Signaling Pathways in the Biology of Classical Hodgkin Lymphoma, Current Molecular Medicine 2011; 11 (3) . https://dx.doi.org/10.2174/156652411795243423
DOI https://dx.doi.org/10.2174/156652411795243423 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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