ReviewHaematologica2026
Translocation t(11;14) and BCL2-inhibition in multiple myeloma.
Review in Haematologica, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 authors.
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Abstract
Multiple myeloma is an increasingly treatable disease with improved survival, although characterized by multiple subclones that drive heterogeneity and variable clinical outcomes between patients. A biomarker-driven approach can help to tailor treatment and improve patient outcomes. Translocation t(11;14), a primary cytogenetic abnormality present in 15-20% of myeloma patients at diagnosis, is currently the most prominent targetable lesion in myeloma. In the era of induction with proteasome inhibitors and/or immunomodulatory drugs, t(11;14) has been associated with poorer outcomes compared to other standard-risk subgroups, with shorter progression-free and overall survival. The presence of t(11;14) in myeloma cells confers increased dependence on the pro-survival BCL2 protein, thus driving its ability to evade apoptosis, and is the main biomarker predicting response to BCL2-inhibitors. This review examines the pathogenesis and prognostic significance of t(11;14) in myeloma and the impact of concurrent high-risk cytogenetics, the mechanism of action of BCL2-inhibitors, cumulative evidence supporting their use, and proposed mechanisms of resistance. The review also presents potential future directions regarding BCL2-inhibitor-based regimens and how best to position these drugs to optimize patient outcomes.
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