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Ghiringhelli, A.

Publications and source records attributed to Ghiringhelli, A..

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The RNA helicase DDX21 cooperates with ETS1 and FLI1 in cell cycle, immune evasion, and snoRNA processing in activated B-cell-like diffuse large B-cell lymphoma cells

Diffuse large B-cell lymphoma (DLBCL) is a clinically and biologically heterogeneous disease, with the activated B-cell-like (ABC) subtype showing inferior outcomes. The ETS transcription factors ETS1 and FLI1 are recurrently gained and functionally relevant in DLBCL, yet their pathogenetic function is still to be fully elucidated. Here, we describe their cooperation with the RNA regulatory machinery, demonstrating that the RNA helicase DDX21 is a central effector of the ETS1/FLI1 transcriptional network in ABC-DLBCL. Our proteomic analyses revealed that ETS1 physically interacted with DDX21 and other RNA processing factors. As ETS1, DDX21 was preferentially expressed in ABC-DLBCL, particularly in the MCD/C5 genetic subtype, and it was associated with adverse clinical outcomes in this lymphoma subtype. Genetic and pharmacological studies demonstrated that DDX21 was essential for ABC-DLBCL cell proliferation. DDX21 also coordinated various transcriptional programs, which were revealed by integrated RNA-Seq, small RNA-Seq, ChIP-Seq, and Capture Hi-C analyses. DDX21-dependent transcription was relevant for ribosome biogenesis, MYC signaling, cell cycle progression, and immune evasion, but also regulated non-coding RNA networks, including microRNAs and small nucleolar RNAs, in particular SNORA37. Collectively, our data establish DDX21 as a nucleolar hub linking ETS transcription factors to coding and non-coding RNA programs that sustain aggressive lymphoma biology. These findings suggest DDX21 and ETS-RNA helicase complexes as promising therapeutic vulnerabilities in ABC-DLBCL.

cancer biology↗

Targeting Aberrant FGFR Signaling with Infigratinib Enhances the Efficacy of BTK/PI3K Inhibitors and Bendamustine in Lymphoma Cells

BackgroundAberrant fibroblast growth factor receptor (FGFR) signaling sustains survival and drug tolerance in various cancers, including B-cell lymphomas. We profiled FGFR/FGF expression and evaluated the FGFR1-3 inhibitor infigratinib, both alone and in combination with standard agents, in models of mantle cell lymphoma (MCL), marginal zone lymphoma (MZL), and diffuse large B-cell lymphoma (DLBCL). MethodsTwenty-eight cell lines (MCL n=10; MZL n=7, including BTK/PI3K inhibitor-resistant derivatives; ABC-DLBCL n=3; GCB-DLBCL n=8) were tested by 72-h MTT assays for single-agent and fixed-ratio combination activity. Transcriptome profiling (4, 8, 12 h) was performed in MZL Karpas1718 cells treated with infigratinib (500 nM), ibrutinib (10 nM), or the combination. ResultsMCL preferentially expressed FGFR3/FGF9, whereas ABC-DLBCL and MZL expressed FGFR1/FGF2; FGFR1 was further enriched in resistant MZL models, consistent with autocrine activation. Infigratinib showed dose-dependent but modest single-agent activity across the panel (median IC50 3.58 M, indicating limited efficacy at clinically achievable exposures ([≤]500 nM). However, combinations were broadly synergistic: in MCL, infigratinib with ibrutinib (4/4 lines) and bendamustine (5/5) outperformed either agent alone, with weaker effects with rituximab (2/4). In MZL (parental and resistant), infigratinib synergized with ibrutinib (6/6), copanlisib (6/6), and idelalisib (4/6), restoring sensitivity in resistant derivatives; synergy occurred at infigratinib concentrations [≤]500 nM. Mechanistically, RNA-seq revealed largely distinct single-agent programs: ibrutinib suppressed BCR/NF-{kappa}B/inflammatory signaling, while infigratinib preferentially repressed E2F/MYC cell-cycle modules. In contrast, the combination concomitantly downregulated NF-{kappa}B pathways and abrogated MYC target signatures, with coordinated modulation of apoptosis and DNA-repair transcripts. ConclusionsFGFR1/3-driven autocrine signaling contributes to adaptive survival in MCL and MZL. Although infigratinib has limited single-agent activity, it potentiates BTK/PI3K inhibitors and bendamustine at clinically relevant concentrations and reverses acquired resistance, supporting biomarker-guided clinical evaluation of FGFR blockade in relapsed/refractory MCL and MZL.

cancer biology↗