test

+|[KLHL14](KLHL14)|Tier 1 GE[@zhangGeneticHeterogeneityDiffuse2013], FE[@choiRegulationCellReceptordependent2020], CE[@hodkinsonBiomarkersResponseIbrutinib2021]|[Zhang et al](papers/zhangGeneticHeterogeneityDiffuse2013)|||

+@article{choiRegulationCellReceptordependent2020,

+ title = {Regulation of {{B}} Cell Receptor-Dependent {{NF-κB}} Signaling by the Tumor Suppressor {{KLHL14}}},

+ author = {Choi, Jaewoo and Phelan, James D. and Wright, George W. and Häupl, Björn and Huang, Da Wei and Shaffer, Arthur L. and Young, Ryan M. and Wang, Zhuo and Zhao, Hong and Yu, Xin and Oellerich, Thomas and Staudt, Louis M.},

+ date = {2020-03-17},

+ journaltitle = {Proceedings of the National Academy of Sciences of the United States of America},

+ shortjournal = {Proc Natl Acad Sci U S A},

+ volume = {117},

+ number = {11},

+ eprint = {32127472},

+ eprinttype = {pmid},

+ pages = {6092--6102},

+ issn = {1091-6490},

+ doi = {10.1073/pnas.1921187117},

+ abstract = {The KLHL14 gene acquires frequent inactivating mutations in mature B cell malignancies, especially in the MYD88L265P, CD79B mutant (MCD) genetic subtype of diffuse large B cell lymphoma (DLBCL), which relies on B cell receptor (BCR) signaling for survival. However, the pathogenic role of KLHL14 in DLBCL and its molecular function are largely unknown. Here, we report that KLHL14 is in close proximity to the BCR in the endoplasmic reticulum of MCD cell line models and promotes the turnover of immature glycoforms of BCR subunits, reducing total cellular BCR levels. Loss of KLHL14 confers relative resistance to the Bruton tyrosine kinase (BTK) inhibitor ibrutinib and promotes assembly of the MYD88-TLR9-BCR (My-T-BCR) supercomplex, which initiates prosurvival NF-κB activation. Consequently, KLHL14 inactivation allows MCD cells to maintain NF-κB signaling in the presence of ibrutinib. These findings reinforce the central role of My-T-BCR-dependent NF-κB signaling in MCD DLBCL and suggest that the genetic status of KLHL14 should be considered in clinical trials testing inhibitors of BTK and BCR signaling mediators in DLBCL.},

+ langid = {english},

+ pmcid = {PMC7084139},

+ keywords = {Adenine,B cell receptor,Carrier Proteins,CD79 Antigens,Cell Line Tumor,DLBCL,Drug Resistance Neoplasm,Endoplasmic Reticulum,Genes Tumor Suppressor,HEK293 Cells,Humans,Intracellular Signaling Peptides and Proteins,KLHL14,Lymphoma Large B-Cell Diffuse,Mutagenesis Site-Directed,Myeloid Differentiation Factor 88,NF-kappa B,NF-κB,Piperidines,Proteolysis,Pyrazoles,Pyrimidines,Receptors Antigen B-Cell,Signal Transduction,Ubiquitin-Protein Ligase Complexes},

+ file = {/Users/rmorin/Zotero/storage/SFDMXWC7/Choi et al. - 2020 - Regulation of B cell receptor-dependent NF-κB sign.pdf}

+}

+

+@article{hodkinsonBiomarkersResponseIbrutinib2021,

+ title = {Biomarkers of Response to Ibrutinib plus Nivolumab in Relapsed Diffuse Large {{B-cell}} Lymphoma, Follicular Lymphoma, or {{Richter}}'s Transformation},

+ author = {Hodkinson, Brendan P. and Schaffer, Michael and Brody, Joshua D. and Jurczak, Wojciech and Carpio, Cecilia and Ben-Yehuda, Dina and Avivi, Irit and Forslund, Ann and Özcan, Muhit and Alvarez, John and Ceulemans, Rob and Fourneau, Nele and Younes, Anas and Balasubramanian, Sriram},

+ date = {2021-01},

+ journaltitle = {Translational Oncology},

+ shortjournal = {Transl Oncol},

+ volume = {14},

+ number = {1},

+ eprint = {33395752},

+ eprinttype = {pmid},

+ pages = {100977},

+ issn = {1936-5233},

+ doi = {10.1016/j.tranon.2020.100977},

+ abstract = {We analyzed potential biomarkers of response to ibrutinib plus nivolumab in biopsies from patients with diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), and Richter's transformation (RT) from the LYM1002 phase I/IIa study, using programmed death ligand 1 (PD-L1) immunohistochemistry, whole exome sequencing (WES), and gene expression profiling (GEP). In DLBCL, PD-L1 elevation was more frequent in responders versus nonresponders (5/8 [62.5\%] vs. 3/16 [18.8\%]; p\,=\,0.065; complete response 37.5\% vs. 0\%; p\,=\,0.028). Overall response rates for patients with WES and GEP data, respectively, were: DLBCL (38.5\% and 29.6\%); FL (46.2\% and 43.5\%); RT (76.5\% and 81.3\%). In DLBCL, WES analyses demonstrated that mutations in RNF213 (40.0\% vs. 6.2\%; p\,=\,0.055), KLHL14 (30.0\% vs. 0\%; p\,=\,0.046), and LRP1B (30.0\% vs. 6.2\%; p\,=\,0.264) were more frequent in responders. No responders had mutations in EBF1, ADAMTS20, AKAP9, TP53, MYD88, or TNFRSF14, while the frequency of these mutations in nonresponders ranged from 12.5\% to 18.8\%. In FL and RT, genes with different mutation frequencies in responders versus nonresponders were: BCL2 (75.0\% vs. 28.6\%; p\,=\,0.047) and ROS1 (0\% vs. 50.0\%; p\,=\,0.044), respectively. Per GEP, the most upregulated genes in responders were LEF1 and BTLA (overall), and CRTAM (germinal center B-cell-like DLBCL). Enriched pathways were related to immune activation in responders and resistance-associated proliferation/replication in nonresponders. This preliminary work may help to generate hypotheses regarding genetically defined subsets of DLBCL, FL, and RT patients most likely to benefit from ibrutinib plus nivolumab.},

+ langid = {english},

+ pmcid = {PMC7723809},

+ keywords = {Biomarkers,Ibrutinib,Nivolumab,Non-hodgkin's lymphoma,Phase I/II trial},

+ file = {/Users/rmorin/Zotero/storage/BQ2G8IID/Hodkinson et al. - 2021 - Biomarkers of response to ibrutinib plus nivolumab.pdf}

+}

+