Author

J. Fassy

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 Pathology· 2

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 3 Research Focus:differential expression· 3 Approach:experimental assay· 3 Organism:mouse· 3 Assay:bulk RNA-seq· 2 Research Focus:drug response / drug discovery· 2 Research Focus:gene regulatory network inference· 2 Organism:human· 2

Frequent Co-Authors

B. Mari· 3 shared G. Vassaux· 3 shared R. Rezzonico· 3 shared A. Baeri· 2 shared C. Cauffiez· 2 shared C. Lacoux· 2 shared G. Savary· 2 shared K. Lebrigand· 2 shared

Activity by Year

2018-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 41 mutual co-author links

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3 shared papersCancer Biology

B. Mari

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

Aging affects reprogramming of murine pulmonary capillary endothelial cells after lung injury

M. Truchi, M. Gautier-Isola, G. Savary, H. Cadis, C. Scribe, A. Baeri, A. Lingampally, V. Magnone, C. Girard-Riboulleau, M.-J. Arguel, C. de Schutter, J. Fassy, N. Boukrout, R. Larrue, N. Martin, , B. Mari

This study compares transcriptomic changes in pulmonary capillary endothelial cells from young and aged mice after lung injury, finding age-related differences in resolution and fibrotic signatures.

bioRxiv · Jul 11, 2023 · PreprintPathology

Processing body dynamics drive non-genetic MEK inhibitors tolerance by fine-tuning KRAS and NRAS translation

O. Vidal-Cruchez, V. J. Nicolini, T. Rete, R. Rezzonico, C. Lacoux, J. Fassy, K. Jacquet, M. A. Domdom, C. Ventujol, T. Juhel, B. Romeo, J. Roux, A. Hubstenberger, B. Mari, B. Mograbi, , P. Brest

The paper identifies a mechanism where MEK inhibitors induce tolerance by promoting KRAS and NRAS translation via PB dissolution, revealing a dynamic feedback loop in MAPK signaling.

bioRxiv · Dec 6, 2021 · PreprintCancer Biology

Blockade of pro-fibrotic response mediated by the miR-143/-145 cluster prevents targeted therapy-induced phenotypic plasticity and resistance in melanoma

S. Diazzi, A. Baeri, J. Fassy, M. Lecacheur, O. Marin-Bejar, C. Girard, L. Lefevre, C. Lacoux, M. Irondelle, C. Mounier, M. Truchi, M. Couralet, A. Carminati, I. Berestjuk, F. Larbret, , S. Tartare-Deckert

This study identifies the miR-143/-145 cluster as a driver of therapy-resistant mesenchymal-like phenotype in melanoma and shows that blocking its pro-fibrotic effects enhances MAPK inhibitor efficacy.

bioRxiv · Jul 2, 2021Cancer Biology

Targeting the DNM3OS / miR-199a~214 cluster for the treatment of fibroproliferative diseases

G. Savary, M. Buscot, E. Dewaeles, S. Diazzi, N. Nottet, E. Courcot, J. Fassy, K. Lebrigand, I. S. Henaoui, N. Martis, C. Van der Hauwaert, S. Leroy, L. Plantier, A. Paquet, C. L. Lino Cardenas, , N. Pottier

This study identifies DNM3OS as a key regulator of fibroblast activation via miRNAs, offering a therapeutic target for fibrotic diseases like IPF.

bioRxiv · Jan 4, 2018 · PreprintPathology