Author

F. Rodier

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· 4 Cell Biology· 2

Signature Assays, Organisms & Methods

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Organism:human· 6 Assay:bulk RNA-seq· 5 Approach:experimental assay· 5 Research Focus:cell type annotation· 4 Research Focus:cancer & tumor microenvironment· 3 Research Focus:chromatin & epigenetic regulation· 2 Research Focus:differential expression· 2 Approach:statistical model· 2

Frequent Co-Authors

N. Malaquin· 4 shared A.-M. Mes-Masson· 3 shared D. Provencher· 3 shared I. Clement· 3 shared K. Rahimi· 3 shared M. Skulimowski· 3 shared A. Martinez· 2 shared E. Carmona· 2 shared

Activity by Year

2018-2023 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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4 shared papersCancer Biology

N. Malaquin

Mutual co-authors in cluster

Author profile →

6 papers

Recent·Most cited

Defining melanoma combination therapies that provide senolytic sensitivity in human melanoma cells

D. Tchelouggou, N. Malaquin, G. B. Cardin, J. Desmul, S. Turcotte, F. Rodier

This study identifies combination therapies for melanoma that enhance senolytic sensitivity by analyzing senescence responses to different treatments.

bioRxiv · Oct 1, 2023Cancer Biology

A senescence-like state is beneficial for ovarian cancer treatment

M. Skulimowski, L. Calvo Gonzalez, S. Cheng, I. Clement, L. Portelance, Y. Zhan, E. Carmona, J. Lafontaine, M. Deladurantaye, K. Rahimi, D. Provencher, A.-M. Mes-Masson, F. Rodier

This study shows that senescence in ovarian cancer cells after chemotherapy correlates with better patient survival, suggesting senescence could be a therapeutic target.

bioRxiv · Sep 30, 2023 · PreprintCancer Biology

53BP1 mediates sensitivity to chemotherapy and is associated with poor clinical outcomes in high-grade serous ovarian cancer

M. Skulimowski, J. Bourbonnais, N. Malaquin, H. Fleury, I. Clement, L. Communal, K. Rahimi, D. Provencher, A.-M. Mes-Masson, F. Rodier

This study shows that high 53BP1 levels in ovarian cancer are linked to poor survival and chemotherapy resistance, suggesting it could be a therapeutic target.

bioRxiv · Sep 30, 2023 · PreprintCancer Biology

Telomeric dysfunction triggers an unstable growth arrest leading to irreparable genomic lesions and entry into cellular senescence

S. Ghadaouia, M.-A. Olivier, A. Martinez, N. Malaquin, G. B. Cardin, F. Rodier

This study shows that telomere uncapping does not directly trigger senescence but leads to genomic instability through telomere fusions and DNA breaks, resulting in irreversible damage.

bioRxiv · Oct 13, 2018 · PreprintCell Biology

Cellular senescence is a central response to cytotoxic chemotherapy in high-grade serous ovarian cancer

L. Calvo, S. Cheng, M. Skulimowski, I. Clement, L. Portelance, Y. Zhan, E. Carmona, J. Lafontaine, M. de Ladurantaye, K. Rahimi, D. Provencher, A.-M. Mes-Masson, F. Rodier

The paper shows that chemotherapy induces cellular senescence in high-grade serous ovarian cancer, which correlates with better patient survival.

bioRxiv · Sep 24, 2018 · PreprintCancer Biology

The NuA4 acetyltransferase and non-canonical chromatin-associated MRN/ATM activity temporally define senescence-associated secretory programs

N. Malaquin, A. Carrier-Leclerc, A. Martinez, M. Dessureault, S. Ghadaouia, J.-P. Coppe, S. Nadeau, G. Cardin, J. Campisi, F. Rodier

The paper shows that delayed recruitment of acetyltransferases and non-canonical DDR activity temporally define SASP in senescence.

bioRxiv · Sep 11, 2018 · PreprintCell Biology