Axel Künstner (@knstnr) header
Axel Künstner (@knstnr) profile picture

Bioinformatician. Statistician. Data squeezer. Omics-addicted with strong focus on #microbiome and #cancer. @knstnr.bsky.social

Lübeck, Germany
Joined April 2018
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Just released EaCoN v0.5.0 "Parallel Universe" 🧬 Modernized the foreach/doParallel → furrr/future + purrr/dplyr migration is complete. R ≥ 4.2 ✅ | OncoScan/CytoScan/SNP6 (hopefully WES) ✅ Fork of the classic @gustaveroussy tool by Bastien Job. github.com/kunstner/EaCoN
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Axel Künstner retweeted
We will soon be hiring postdocs, engineers and researchers (on site in Heidelberg, DE) in: - Biomedical AI (multimodal foundation models, biomarkers, agents) - Robotics (lab automation, physical action surfaces for agents) - AI social sciences (multi-agent systems, agent "civilizations") - Deploying AI in a large hospital system More info at imai-heidelberg.de and kather.ai If you are interested in learning more, reach out to [email protected]
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1/8 🦠🍃 New paper in npj Systems Biology and Applications! Chronic otitis media (COM) is a leading cause of preventable hearing loss. We asked: can the natural anti-inflammatory compound 1,8-Cineol reshape the ear microbiome beyond antibiotics? 🧵 nature.com/articles/s41540-0…
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7/8 Bottom line: diversity indices alone can miss real ecological restructuring. Network analysis uncovers hidden shifts in host-associated microbiomes and points to new therapeutic/biomarker targets for COM.
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Great teamwork with @UniLuebeck & @UKSH_official (ENT, Infectious Diseases/Microbiology & Systems Biology). Open access, data at EGA (PRJEB104438), code included. #Microbiome #Mycobiome #OtitisMedia #NetworkAnalysis #OpenAccess
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🧬 New paper! Within #InstandNGS4P we developed MRD prototypes detecting ctDNA in blood plasma to support diagnosis of pancreatic & ovarian cancer — UMI-based error correction + ultra-deep sequencing. 📄 @OpenResearch_EU: open-research-europe.ec.euro… #LiquidBiopsy #ctDNA
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United we stand, divided we fall.
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🧬 New in Blood: we describe FOXF1/FENDRR — a novel molecular subtype of B-cell precursor ALL in adults, found in 20/4857 patients across 3 cohorts. Defined by a previously unknown IGH::FENDRR rearrangement + recurrent KRAS mutations (p.A146V/T/P). 🧵 doi.org/10.1182/blood.202503…
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Clinically, this subtype responds poorly to standard chemo: most patients had induction failure or MRD persistence. But intensification with blinatumomab and/or allo-HSCT rescued the majority — pointing to early immunotherapy as a promising strategy.
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A gene expression classifier built accurately flags FOXF1/FENDRR cases in independent cohorts (GRAALL, St. Jude), so this subtype can now be systematically identified in routine diagnostics. Grateful to the whole @UKSH_KI_HL team and collaborators! 📄
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New in Blood @BloodPortfolio lenalidomide (maintenance tx in myeloma) raises B-ALL risk. We show WHY in a subset of cases IDH2 R140Q clonal hematopoiesis + lenalidomide-driven IKAROS loss cooperate to arrest B-cell development, seeding a distinct leukemia subtype. 🧵
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DNA methylation profiling revealed IDH2mt LenB-ALL has its own hypermeth. phenotype, distinct from primary B-ALL. Epigenetic evidence backing up the mutational story. IDH2 mutations were even detectable in remission, pointing to a preleukemic origin. doi.org/10.1182/blood.202503…
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Preprint: In PD-L1-gain EBV+ DLBCL, T cells get close to tumour cells but rarely touch them; a spatial "decoupling" of proximity and engagement. Fibroblast barriers, metabolic suppression, and T cell exhaustion together block anti-tumour immunity. 🧵1/5 doi.org/10.64898/2026.07.02.…
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Even T cells that do get close are functionally silenced (exhaustion markers up, metabolic suppression signatures enriched, effector programs down). It's a two-layer fortress: physical exclusion + functional suppression working together. 4/5
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This "fortress model" offers a new lens on PD-L1–driven immune evasion in EBV+ DLBCL, and may help explain variable responses to checkpoint blockade in this subtype. Preprint + full methods + data 5/5
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