Author

H. A. Armelin

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

Biology Disciplines

Click to filter author papers

Cancer Biology· 2

Signature Assays, Organisms & Methods

Click to filter · or open tag

Research Focus:cancer & tumor microenvironment· 2 Approach:experimental assay· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:drug response / drug discovery· 1 Organism:mouse· 1 Research Focus:perturbation response prediction· 1 Assay:proteomics· 1

Frequent Co-Authors

M. H. Dias· 2 shared M. S. da Silva· 2 shared A. Dekker· 1 shared A. Friskes· 1 shared A. Mulero-Sanchez· 1 shared A. van Oudenaarden· 1 shared A. Vidal· 1 shared A. Villanueva· 1 shared

Activity by Year

2018-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

2 shared papersCancer Biology

M. H. Dias

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Paradoxical activation of oncogenic signaling as a cancer treatment strategy

M. H. Dias, A. Friskes, S. Wang, J. M. H. Fernandes Neto, F. v. Gemert, S. Mourragui, H. J. Kuiken, S. Mainardi, D. Alvarez-Villanueva, C. Lieftink, B. Morris, A. Dekker, E. v. Dijk, C. Papagianni, M. S. da Silva, , R. Bernards

This study shows that inhibiting PP2A and WEE1 together can kill colon cancer cells by causing DNA replication collapse and cell death, and that resistance to this treatment suppresses tumor growth.

bioRxiv · Feb 6, 2023Cancer Biology

Fibroblast Growth Factor 2 lethally sensitizes cancer cells to stress-targeted therapeutic inhibitors

M. H. Dias, C. S. Fonseca, J. D. Zeidler, L. L. Albuquerque, M. S. da Silva, E. Cararo-Lopes, M. S. Reis, V. Noel, I. A. Prior, H. A. Armelin

This study shows that FGF2 sensitizes cancer cells to stress-targeted therapies by disrupting homeostasis and inducing synthetic lethal interactions with proteasome or DNA damage inhibitors.

Molecular Oncology · Dec 3, 2018Peer-reviewedCancer Biology