Author

J.-C. Bourdon

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cancer Biology· 3

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell type annotation· 2 Assay:bulk RNA-seq· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

A. Carrapeiro· 1 shared A. Fajac· 1 shared A. Hamon· 1 shared A. Kind· 1 shared A. Morillon· 1 shared A. Morin· 1 shared A. Poteete· 1 shared A. Schnieke· 1 shared

Activity by Year

2020-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 16 mutual co-author links

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1 shared paperCancer Biology

A. Carrapeiro

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Author profile →

3 papers

Recent·Most cited

Mutant mice lacking alternatively spliced p53 isoforms unveil Ackr4 as a male-specific prognostic factor in Myc-driven B-cell lymphomas

A. Fajac, I. Simeonova, J. Leemput, M. Gabriel, A. Morin, V. Lejour, A. Hamon, J. Rakotopare, W. Vaysse-Zinkhofer, E. Eldawra, M. Pinskaya, A. Morillon, J.-C. Bourdon, B. Bardot, F. Toledo

The paper shows that male-specific protection against Myc-driven B-cell lymphomas is lost in mice lacking alternatively spliced p53 isoforms, identifying Ackr4 as a prognostic factor.

bioRxiv · Oct 13, 2023Cancer Biology

Porcine model elucidates function of p53 isoform in carcinogenesis

G. Niu, I. Hellmuth, T. Flisikowska, H. Pausch, B. Rieblinger, A. Carrapeiro, B. Schade, B. Boehm, E. Kappe, K. Fischer, B. Klinger, K. Steiger, D. Saur, J.-C. Bourdon, R. Burgkart, , K. Flisikowski

This study uses a porcine model to show that specific p53 isoforms and circular TP53 RNA drive tumorigenesis, particularly osteosarcoma, in pigs and likely have similar roles in humans.

bioRxiv · Sep 7, 2020 · PreprintCancer Biology

Inhibition of nonsense-mediated decay rescues functional p53β/γ isoforms in MDM2-amplified cancers

J. P. Gudikote, T. Cascone, A. Poteete, P. Sitthideatphaiboon, Q. Wu, N. Morikawa, F. Zhang, S. Peng, P. Tong, L. Li, L. Shen, M. Nilsson, P. Jones, E. P. Sulman, J. Wang, , J. Heymach

The paper shows that inhibiting nonsense-mediated decay increases expression of p53β/γ isoforms, which are resistant to MDM2 degradation, thereby restoring p53 function in cancers with MDM2 amplification, HPV infection, or specific p53 mutations.

bioRxiv · Apr 6, 2020 · PreprintCancer Biology