Author

Branka Radic-Sarikas

St. Anna Children's Cancer Research InstituteORCID 0000-0002-3597-0483Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cancer Biology· 3

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 3 Approach:experimental assay· 3 Research Focus:differential expression· 2 Research Focus:drug response / drug discovery· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1

Frequent Co-Authors

Florian HalbritteriD· 3 shared Heinrich KovariD· 3 shared Martha Magdalena ZylkaiD· 2 shared Martin Lothar MetzelderiD· 2 shared Veveeyan SureshiD· 2 shared Aleksandr BykoviD· 1 shared Aleksandr OvsianikoviD· 1 shared Antonin MarchaisiD· 1 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 32 mutual co-author links

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3 shared papersCancer Biology

Florian HalbritterORCID

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3 papers

Recent·Most cited

Cancer BiologybioRxivPreprintJun 8, 2026

A human lung organoid co-culture model of early bone sarcoma metastasis reveals contact-dependent epithelial remodeling at the metastatic interface

Martha Magdalena Zylka, Tümay Capraz, Gaël Moquin‐Beaudry…·Branka Radic-Sarikas

This paper introduces a 3D co-culture model of bone sarcoma metastasis in the lung and identifies a contact-dependent epithelial remodeling response with potential therapeutic targets.

DOI 10.64898/2026.06.03.729838

humanspatial transcriptomics

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Cancer BiologyMolecular Therapy OncologyPeer-reviewedMay 9, 2026

Mevalonate pathway activation in Ewing sarcoma reveals a 3D-specific synergy between statins and BCL-xL inhibition

Branka Radic-Sarikas, Marica Marković, Martha Magdalena Zylka…·Heinrich Kovar

The paper develops a 3D culture platform for Ewing sarcoma and identifies a synergy between statins and BCL-xL inhibitors targeting the mevalonate pathway.

DOI 10.1016/j.omton.2026.201229

humanbulk RNA-seq

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Cancer BiologyCell ReportsPeer-reviewedMar 1, 2025

YAP1 is a key regulator of EWS::FLI1-dependent malignant transformation upon IGF-1 mediated reprogramming of bone mesenchymal stem cells

Rahil Noorizadeh, Barbara Sax, Tahereh Javaheri…·Heinrich Kovar

The paper shows that IGF-1 reprograms bone mesenchymal stem cells in EWS::FLI1-mutant mice, leading to tumor formation, with Yap1 playing a central role, and suggests combined IGF-1R and YAP/TEAD inhibition as a potential treatment.

11 citations

mouseexperimental assay

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