ArticleVeterinary and comparative oncology2026
Cross-Species Transcriptomic and Network Analysis of Human and Canine Diffuse Large B-Cell Lymphoma Identifies a Conserved Replication-DNA Damage Module for Drug Repurposing.
Article in Veterinary and comparative oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Rational, mechanism-based drug selection for canine diffuse large B-cell lymphoma (DLBCL) remains limited, despite extensive molecular work in human DLBCL. We asked whether human and canine DLBCL share a conserved transcriptional network that could anchor therapeutic hypotheses for dogs. Using public human and canine DLBCL transcriptomes, we derived a 409-gene cross-species module defined by concordant tumour-normal dysregulation and projected it onto pathway and protein-protein interaction (PPI) networks. The module was dominated by DNA replication, cell-cycle checkpoint and DNA damage-response programmes and contained a compact PPI core centred on TOP2A and PARP1. Querying the Connectivity Map/LINCS library with the human component of the module highlighted anthracycline-like topoisomerase II poisons (valrubicin, etoposide, amsacrine) and the PARP inhibitor rucaparib among the ~0.2% most negative connectivity scores, while directly targeting TOP2A and/or PARP1. A simple up-down module score strongly separated tumour from normal lymph nodes in both species and was associated with outcome: higher scores predicted longer progression-free survival in CHOP-treated dogs and better overall survival in an independent human cohort, with a similar but underpowered trend in TCGA-DLBC. Finally, extracellular-vesicle microRNA (EV-miRNA) profiling in human DLBCL showed that differentially expressed EV-miRNAs, including let-7 family members, miR-21-5p, miR-124-3p and miR-205-5p, converge on the same TOP2A/PARP1-centred core. These cross-species, multi-layer data support topoisomerase II poisons and PARP inhibition as coherent, network-anchored candidate therapies for canine DLBCL, with module scores and EV-miRNAs as candidate biomarkers.
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