ArticleAnnals of hematology2026
Transcriptomic profiling of an in vivo diffuse large B-cell lymphoma model reveals molecular programs underlying CNS dissemination.
Article in Annals of hematology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
12 authors.
Funding
Abstract
Secondary central nervous system involvement (sCNSi) is a fatal complication of diffuse large B-cell lymphoma (DLBCL), yet its molecular determinants remain poorly understood. To investigate the mechanisms underlying CNS-preferential dissemination, we established an in vivo DLBCL xenograft model using two representative cell lines, OCI-LY19 and Toledo, followed by transcriptomic profiling of lymphoma cells isolated from the brain, peripheral organs, and parental cultures. Transcriptomic analyses revealed gene signatures associated with CNS-preferential dissemination, which were further evaluated in RNA-seq data from diagnostic tissues of patients with (n = 19) or without (n = 16) sCNSi. CNS tropism of DLBCL cells was associated with increased expression of genes involved in PI3K-Akt-mTOR and ARF6 trafficking signaling and decreased expression of sphingosine-1-phosphate receptor signaling. Patient-derived transcriptomes exhibited enrichment of pathways that were functionally related to the gene signatures observed in the xenograft model. These findings suggest that CNS-preferential dissemination in DLBCL is associated with coordinated signaling involving PI3K/ARF6 activation and suppression of S1P-mediated pathways, providing molecular insights with potential implications for risk stratification and therapeutic targeting in sCNSi.
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