Author

A. Janic

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

Signature Assays, Organisms & Methods

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Assay:ATAC-seq· 1 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Approach:experimental assay· 1 Organism:human· 1 Organism:mouse· 1 Approach:statistical model· 1

Frequent Co-Authors

A. Ganez-Zapater· 1 shared A. Strasser· 1 shared C. Cannata· 1 shared D. Datta· 1 shared F. Pezzano· 1 shared G. Healey· 1 shared J. Urgel-Solas· 1 shared K. Brinkmann· 1 shared

Activity by Year

2023-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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1 shared paperCancer Biology

A. Ganez-Zapater

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2 papers

Recent·Most cited

Combined absence of TRP53 target genes ZMAT3, PUMA and p21 cause a high incidence of cancer in mice

A. Janic, A. Strasser, M. Herold, M. S. Brennan, G. Healey, L. Gangoda, K. Brinkmann

The paper shows that combined absence of TRP53 target genes ZMAT3, PUMA, and p21 in mice leads to a higher incidence of cancer, with different tumor types depending on which genes are missing.

Cell Death & Differentiation · Dec 18, 2023Peer-reviewedCancer Biology

Adaptation to ARF6-depletion in KRAS-driven PDAC is abolished by targeting TLR2

R. Ghose, S. Das, J. Urgel-Solas, F. Pezzano, D. Datta, U. Ghose, A. Ganez-Zapater, N. Pardo-Lorente, L. Espinar, L. Garcia, C. Cannata, V. Ruprecht, A. Janic, S. Sdelci

This study identifies TLR2 as a target to counteract adaptation to ARF6 depletion in KRAS-driven PDAC, reducing proliferation, migration, and invasion.

bioRxiv · Nov 30, 2023 · PreprintCancer Biology