Author

Fei Song

Institute of Cancer ResearchORCID 0000-0002-3286-8782Unclaimed ORCID profile · follow to get notified of new preprints

Additional preprints under this name without ORCID

Fei Song1 paper · Beijing Normal University

Biology Disciplines

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Cancer Biology· 1 Genomics· 1

Signature Assays, Organisms & Methods

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Research Focus:differential expression· 2 Research Focus:gene regulatory network inference· 2 Research Focus:cell type annotation· 1 Approach:experimental assay· 1 Organism:human· 1 Organism:mouse· 1 Approach:statistical model· 1 Research Focus:variant calling· 1

Frequent Co-Authors

Andrew N.J. TuttiD· 2 shared Christopher J. LordiD· 2 shared Dragomir B. KrasteviD· 2 shared Rachel BroughiD· 2 shared Stephen J. PettittiD· 2 shared Amaury VaysseiD· 1 shared Andrea DegasperiiD· 1 shared Aurélien BoreiD· 1 shared

Activity by Year

2026-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 39 mutual co-author links

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2 shared papersGenomics

Andrew N.J. TuttORCID

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2 papers

Recent·Most cited

Global signatures of Ribonucleotide Excision Repair deficiency and its therapeutic vulnerabilities

Ping Jing Toong, Soraya Boushaki, Salome Jingchen Zhao, Rachel Brough, Fei Song, Dragomir B. Krastev, Daniella Black, Giuseppe Rinaldi, Cherif Badja, Andrea Degasperi, Jan Czarnecki, Yasin Memari, Helen Davies, Daniel Hüebschmann, Hanno Glimm, , Serena Nik‐Zainal

This study identifies RER deficiency as a new DNA repair defect in cancer, detectable through mutational signatures and linked to therapeutic vulnerabilities.

bioRxiv · Oct 15, 2026 · PreprintGenomics

The FANCM-RMI1/2 complex promotes genomic instability and PARP inhibitor sensitivity in BRCA2-deficicient cells.

François Dossin, Mikaël Attia, Fabricio Montero Zuniga, Daniel González‐Acosta, Rachel Brough, Fei Song, Dragomir B. Krastev, Maya Raghunandan, Stephen J. Pettitt, Aurélien Bore, Amaury Vaysse, Raphaël Margueron, Massimo Lopes, Andrew N.J. Tutt, Christopher J. Lord, Ludovic Deriano

This study identifies FANCM-RMI1/2 as a driver of PARP inhibitor sensitivity in BRCA2-deficient cells, revealing distinct adaptation mechanisms between BRCA1 and BRCA2 loss.

Molecular Cell · Oct 1, 2026Peer-reviewedCancer Biology