Přehled o publikaci

The presence of either TP53 gene loss or mutation defined high-risk CLL especially in the era of chemoimmunotherapy. Its prognostic and predictive impact remains a matter of debate in the setting of BTKi- and BCL2i-based treatment, which does not act directly via the TP53 pathway, but yet seems to associate with worse clinical outcomes. The adverse effect on overall survival, at least upon chemoimmunotherapy, is notable not only in patients with expanded but also in lowburden TP53 mutations, which were identified in 5–35% of CLL patients. In this study, we aimed to scrutinize the principles of clonal competition in CLL and identify factors influencing the development of TP53-mutated subclones in various clinical contexts.