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Related Experiment Video

Updated: Oct 25, 2025

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Kinobead Profiling Reveals Reprogramming of BCR Signaling in Response to Therapy within Primary CLL Cells.

Adam J Linley1, Laura I Karydis2, Anil K Mondru3

  • 1Department of Molecular Physiology and Cell Signaling, Institute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, United Kingdom. a.linley@liverpool.ac.uk.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|August 12, 2021
PubMed
Summary

This study reveals how chronic lymphocytic leukemia (CLL) cells adapt their B-cell receptor (BCR) signaling in response to therapy. Understanding these adaptive changes is key for developing new treatments targeting BCR signaling in CLL patients.

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Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • B-cell receptor (BCR) signaling is crucial for chronic lymphocytic leukemia (CLL) pathogenesis, driving malignant cell survival and progression.
  • The broader signaling network in BCR-stimulated CLL cells remains poorly understood, especially concerning therapeutic interventions like kinase inhibitors.

Purpose of the Study:

  • To develop a novel high-resolution method for investigating BCR signaling in primary CLL cells.
  • To track how therapy influences the BCR signaling response in CLL cells.

Main Methods:

  • Utilized a kinobead/mass spectrometry-based protocol to analyze BCR signaling in primary CLL cells.
  • Conducted longitudinal analysis of clinical trial patient samples to assess the impact of chemoimmunotherapy and ibrutinib.
  • Employed Nanostring and immunoblotting for verification of findings.

Main Results:

  • Identified patient-specific BCR signaling signatures involving over 30 kinases and 13 KEGG pathways.
  • Observed significant alterations in these signaling signatures between treatment-naïve and previously treated CLL patients.
  • Validated changes in BCR-induced kinome responses longitudinally, correlating with disease progression or ibrutinib treatment.

Conclusions:

  • Presents the first comprehensive proteomic investigation of BCR signaling response in CLL cells.
  • Provides novel evidence of adaptive reprogramming of BCR signaling in CLL cells following therapy.
  • Highlights the potential for targeting these adaptive signaling changes in CLL treatment.