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December 8, 2025BloodOpen Access

Genomic profiling in CLL patients after BTK inhibitor progression identifies enrichment of mutations in MAPK pathway and epigenetic regulators

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Authors

DLDaniela Trujillo LoaizaEBEsteban Braggio

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Overview

Analysis demonstrates prevalence of mutations in epigenetic regulators and the MAPK pathway in CLL patients, suggesting distinct resistance mechanisms.

Key Points

  • Disease progression linked to mutations in epigenetic regulators and MAPK pathway.
  • Prior to treatment, common abnormalities included del13q in 65% and TP53 mutations in 59%.
  • Observational analysis of RR CLL patients employed whole genome sequencing on 64 blood samples for genomic profiling.
  • Findings highlight that resistance mechanisms extend beyond BTK and PLCG2, indicating complex genomic evolution.

Cite This Study

Loaiza et al. (2025) studied this question.

synapsesocial.com/papers/69362f4e4fa91c937236d8b6https://doi.org/10.1182/blood-2025-5660
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Clonal architecture and growth dynamics of ibrutinib-resistant CLL: Oligoclonal BTK/PLCG2 mutations and emerging non-BTK/PLCG2 drivers2025 · 1 citations
  2. 2Systematic molecular profiling to identify determinants of response to ibrutinib2025
  3. 3Acquired Bruton's tyrosine kinase mutations in patients treated on the ibrutinib and rituximab, ibrutinib alone, and ibrutinib and venetoclax arms of the national multi-centre Phase III FLAIR study in previously untreated CLL patients2025 · 3 citations
  4. 4Efficacy and prognostic determinants of BTK inhibitors in chronic lymphocytic leukemia (CLL): A real-world single-center cohort study from China2025
  5. 5Resistance Mutations in CLL: Genetic Mechanisms Shaping the Future of Targeted Therapy2025