Aberrant splicing of the tumor suppressor CYLD promotes the development of chronic lymphocytic leukemia via sustained NF-κB signaling View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2018-01

AUTHORS

M Hahn, J-P Bürckert, C A Luttenberger, S Klebow, M Hess, M Al-Maarri, M Vogt, S Reißig, M Hallek, A Wienecke-Baldacchino, T Buch, C P Muller, C P Pallasch, F T Wunderlich, A Waisman, N Hövelmeyer

ABSTRACT

The pathogenesis of chronic lymphocytic leukemia (CLL) has been linked to constitutive NF-κB activation but the underlying mechanisms are poorly understood. Here we show that alternative splicing of the negative regulator of NF-κB and tumor suppressor gene CYLD regulates the pool of CD5+ B cells through sustained canonical NF-κB signaling. Reinforced canonical NF-κB activity leads to the development of B1 cell-associated tumor formation in aging mice by promoting survival and proliferation of CD5+ B cells, highly reminiscent of human B-CLL. We show that a substantial number of CLL patient samples express sCYLD, strongly implicating a role for it in human B-CLL. We propose that our new CLL-like mouse model represents an appropriate tool for studying ubiquitination-driven canonical NF-κB activation in CLL. Thus, inhibition of alternative splicing of this negative regulator is essential for preventing NF-κB-driven clonal CD5+ B-cell expansion and ultimately CLL-like disease. More... »

PAGES

72

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/leu.2017.168

DOI

http://dx.doi.org/10.1038/leu.2017.168

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1085744865

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28566736


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