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+@article{mansouriFunctionalLossIkBe2015,

+ title = {Functional Loss of {{IκBε}} Leads to {{NF-κB}} Deregulation in Aggressive Chronic Lymphocytic Leukemia},

+ author = {Mansouri, Larry and Sutton, Lesley-Ann and Ljungström, Viktor and Bondza, Sina and Arngården, Linda and Bhoi, Sujata and Larsson, Jimmy and Cortese, Diego and Kalushkova, Antonia and Plevova, Karla and Young, Emma and Gunnarsson, Rebeqa and Falk-Sörqvist, Elin and Lönn, Peter and Muggen, Alice F. and Yan, Xiao-Jie and Sander, Birgitta and Enblad, Gunilla and Smedby, Karin E. and Juliusson, Gunnar and Belessi, Chrysoula and Rung, Johan and Chiorazzi, Nicholas and Strefford, Jonathan C. and Langerak, Anton W. and Pospisilova, Sarka and Davi, Frederic and Hellström, Mats and Jernberg-Wiklund, Helena and Ghia, Paolo and Söderberg, Ola and Stamatopoulos, Kostas and Nilsson, Mats and Rosenquist, Richard},

+ date = {2015-06-01},

+ journaltitle = {The Journal of Experimental Medicine},

+ shortjournal = {J Exp Med},

+ volume = {212},

+ number = {6},

+ eprint = {25987724},

+ eprinttype = {pmid},

+ pages = {833--843},

+ issn = {1540-9538},

+ doi = {10.1084/jem.20142009},

+ abstract = {NF-κB is constitutively activated in chronic lymphocytic leukemia (CLL); however, the implicated molecular mechanisms remain largely unknown. Thus, we performed targeted deep sequencing of 18 core complex genes within the NF-κB pathway in a discovery and validation CLL cohort totaling 315 cases. The most frequently mutated gene was NFKBIE (21/315 cases; 7\%), which encodes IκBε, a negative regulator of NF-κB in normal B cells. Strikingly, 13 of these cases carried an identical 4-bp frameshift deletion, resulting in a truncated protein. Screening of an additional 377 CLL cases revealed that NFKBIE aberrations predominated in poor-prognostic patients and were associated with inferior outcome. Minor subclones and/or clonal evolution were also observed, thus potentially linking this recurrent event to disease progression. Compared with wild-type patients, NFKBIE-deleted cases showed reduced IκBε protein levels and decreased p65 inhibition, along with increased phosphorylation and nuclear translocation of p65. Considering the central role of B cell receptor (BcR) signaling in CLL pathobiology, it is notable that IκBε loss was enriched in aggressive cases with distinctive stereotyped BcR, likely contributing to their poor prognosis, and leading to an altered response to BcR inhibitors. Because NFKBIE deletions were observed in several other B cell lymphomas, our findings suggest a novel common mechanism of NF-κB deregulation during lymphomagenesis.},

+ langid = {english},

+ pmcid = {PMC4451125},

+ keywords = {Cell Nucleus,Cell Survival,Chromosome Aberrations,Cohort Studies,Cytoplasm,DNA Mutational Analysis,Frameshift Mutation,Gene Deletion,Gene Expression Profiling,Gene Expression Regulation Leukemic,Humans,I-kappa B Kinase,Leukemia Lymphocytic Chronic B-Cell,Lymphoma B-Cell,Lymphoma B-Cell Marginal Zone,Lymphoma Mantle-Cell,NF-kappa B,Oligonucleotide Array Sequence Analysis,Receptors Antigen B-Cell,Signal Transduction,Treatment Outcome},

+ file = {/Users/rmorin/Zotero/storage/IFEN6256/Mansouri et al. - 2015 - Functional loss of IκBε leads to NF-κB deregulatio.pdf}

+}

+

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