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September 5, 2025Open Access

Inhibition of autoantigen-induced B-cell receptor (BCR) internalization as a therapeutic strategy in Diffuse Large B Cell Lymphoma (DLBCL)

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Authors

PGPatryk GórniakAPAnna PolakARAnna Rams

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Overview

Mechanistic insights on B-cell receptor signaling in DLBCL reveal autoantigen implications for therapy.

Key Points

  • Inhibition of BCR internalization is crucial for reducing signaling in DLBCL.
  • Autoantigens facilitate the formation of the BCR-TLR9-IκB complex, promoting oncogenic signaling.
  • Using CRISPR-Cas9, models demonstrated that modified BCRs could not bind self-antigens.
  • CME inhibition with phenothiazine derivatives reduces cell viability and synergizes with SYK and PI3Kδ inhibitors.

Cite This Study

Górniak et al. (2025) studied this question.

synapsesocial.com/papers/68c239a3b210217d6477d6f2https://doi.org/10.21203/rs.3.rs-7260543/v1
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Also Consider

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  1. 1Autonomous BCR signaling and the CARD11 L251P mutation as alternative oncogenic drivers induce identical gene expression profiles in genetically engineered ABC-DLBCL models2025
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  3. 3Adenosine pathway as a therapeutic target in diffuse large B cell lymphoma2025
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