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Transcriptomic profiling of an in vivo diffuse large B-cell lymphoma model reveals molecular programs underlying CNS
So-Jeong Kim1,2, Hyo-Kyung Pak1,3, Hyunji Kim1,3
1Department of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 05505, Republic of Korea.
Annals of Hematology
|July 1, 2026
Summary
Diffuse large B-cell lymphoma (DLBCL) can spread to the central nervous system (CNS). This study identifies key molecular pathways, including PI3K/ARF6 signaling, involved in DLBCL
Area of Science:
- Oncology
- Molecular Biology
- Neuroscience
Background:
- Secondary central nervous system involvement (sCNSi) is a fatal complication of diffuse large B-cell lymphoma (DLBCL).
- The molecular mechanisms driving CNS-preferential dissemination in DLBCL are not well understood.
Purpose of the Study:
- To investigate the molecular determinants of CNS-preferential dissemination in DLBCL.
- To identify potential therapeutic targets for sCNSi.
Main Methods:
- Established an in vivo DLBCL xenograft model using OCI-LY19 and Toledo cell lines.
- Performed transcriptomic profiling of lymphoma cells from the brain, peripheral organs, and parental cultures.
- Evaluated gene signatures in RNA-seq data from DLBCL patient tissues with or without sCNSi.
Main Results:
- Identified gene signatures associated with CNS-preferential dissemination in DLBCL.
- Found increased expression of PI3K-Akt-mTOR and ARF6 trafficking signaling genes.
- Observed decreased expression of sphingosine-1-phosphate receptor signaling in CNS-tropism.
Conclusions:
- CNS-preferential dissemination in DLBCL is linked to coordinated PI3K/ARF6 activation and S1P pathway suppression.
- These findings offer molecular insights for risk stratification and therapeutic targeting of sCNSi in DLBCL.
