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In This Issue| September 03 2024 Highlighted research articles Author 5 (5): 302. https://doi.org/10.1158/2643-3230.BCD-5-5-ITI Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest Search Advanced Search Aberrant turnover of cellular proteins can drive lymphomagenesis. Kelch-like family member 6 (KLHL6) encodes a substrate-determining module for a powerful protein degradation machinery with undetermined targets, and it is recurrently mutated in diffuse large B-cell lymphoma (DLBCL). By applying high-throughput proteomic screens and functional studies, Meriranta and colleagues revealed that KLHL6 targets and downregulates B-cell receptor (BCR). In B cells, selected KLHL6 mutants localized abnormally, resulting in elevated plasma membrane BCR levels that fueled BCR signaling. Loss of KLHL6 expression characterized activated B-cell–like DLBCLs with poor outcomes and associated with a targetable phenotype with high BCR levels. See article, p. 331. With axicabtagene ciloleucel (axi-cel) and tisagenlecleucel (tisa-cel) now approved for large B-cell lymphoma (LBCL), criteria for choosing the optimal CAR T-cell therapy become a pressing clinical question. Stella and colleagues tackle it in a real-life prospective study spanning 21 institutions, matching baseline characteristics of 485 patients... You do not currently have access to this content.
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