ArticleFrontiers in oncology2026
Bcl-2 inhibitor resistance in diffuse large b-cell lymphoma: establishing a prognostic signature and targeting alpha protein kinase 1.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Drug resistance in diffuse large B-cell lymphoma (DLBCL) contributes to poor prognosis in 30-40% of newly diagnosed patients in the era of first-line rituximab combined with cyclophosphamide, doxorubicin, vincristine, and prednisone therapy. Targeting Bcl-2 has been shown to target for improve the prognosis of these patients, based on the clinical trials of its inhibitor, venetoclax. However, venetoclax resistance in DLBCL remains a challenge. Methods: The 'WGCNA' package was used to comprehensively screen for Bcl-2 inhibitor-resistant genes (Bcl-2RGs) and the Bcl-2RGs signature was established using LASSO regression analysis with ten-fold cross-validation. Results: The Bcl-2 signature is an effective prognostic prediction model using Gene Expression Omnibus data analysis. In addition, we demonstrated that the inhibition of alpha protein kinase 1 (ALPK1) decreased the proliferation of DLBCL cells and increased apoptosis. ALPK1 inhibitor treatment synergized with venetoclax to suppress the ALPK1/NFκB signaling pathway. Conclusion: Overall, we showed that the Bcl-2 signature could predict the prognosis of patients with DLBCL, and that ALPK1 could be a promising target for sensitizing patients with DLBCL to venetoclax therapy. Methods: The 'WGCNA' package was used to comprehensively screen for Bcl-2 inhibitor-resistant genes (Bcl-2RGs) and the Bcl-2RGs signature was established using LASSO regression analysis with ten-fold cross-validation. Results: The Bcl-2 signature is an effective prognostic prediction model using Gene Expression Omnibus data analysis. In addition, we demonstrated that the inhibition of alpha protein kinase 1 (ALPK1) decreased the proliferation of DLBCL cells and increased apoptosis. ALPK1 inhibitor treatment synergized with venetoclax to suppress the ALPK1/NFκB signaling pathway. Conclusion: Overall, we showed that the Bcl-2 signature could predict the prognosis of patients with DLBCL, and that ALPK1 could be a promising target for sensitizing patients with DLBCL to venetoclax therapy. Results: The Bcl-2 signature is an effective prognostic prediction model using Gene Expression Omnibus data analysis. In addition, we demonstrated that the inhibition of alpha protein kinase 1 (ALPK1) decreased the proliferation of DLBCL cells and increased apoptosis. ALPK1 inhibitor treatment synergized with venetoclax to suppress the ALPK1/NFκB signaling pathway. Conclusion: Overall, we showed that the Bcl-2 signature could predict the prognosis of patients with DLBCL, and that ALPK1 could be a promising target for sensitizing patients with DLBCL to venetoclax therapy. Conclusion: Overall, we showed that the Bcl-2 signature could predict the prognosis of patients with DLBCL, and that ALPK1 could be a promising target for sensitizing patients with DLBCL to venetoclax therapy.
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