Author

N. Malaquin

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· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

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Organism:human· 3 Assay:bulk RNA-seq· 2 Research Focus:cancer & tumor microenvironment· 2 Approach:experimental assay· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:clustering· 1

Frequent Co-Authors

F. Rodier· 3 shared G. B. Cardin· 2 shared A. Martinez· 1 shared A.-M. Mes-Masson· 1 shared D. Provencher· 1 shared D. Tchelouggou· 1 shared H. Fleury· 1 shared I. Clement· 1 shared

Activity by Year

2018-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 23 mutual co-author links

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3 shared papersCancer Biology

F. Rodier

Mutual co-authors in cluster

Author profile →

3 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

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