Author

S. Mittnacht

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· 3

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 3 Organism:human· 3 Assay:bulk RNA-seq· 2 Research Focus:drug response / drug discovery· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1

Frequent Co-Authors

G. Zoumpoulidou· 2 shared S. J. Strauss· 2 shared A. De Haven Brandon· 1 shared A. Hayes· 1 shared B. Al-Lazikani· 1 shared C. A. Mendoza· 1 shared C. Alvarez-Mendoza· 1 shared C. D. Steele· 1 shared

Activity by Year

2019-2020 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 18 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

G. Zoumpoulidou

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Therapeutic vulnerability to PARP1/2 inhibition in RB1-mutant osteosarcoma

G. Zoumpoulidou, C. A. Mendoza, C. Mancusi, R. M. Ahmed, M. Denman, C. D. Steele, J. Manji, N. Pillay, S. J. Strauss, S. Mittnacht

This study shows RB1-mutant osteosarcoma is hypersensitive to PARP1/2 inhibitors, with sensitivity linked to replication checkpoint activation rather than homologous repair defects.

bioRxiv · Dec 28, 2020 · PreprintCancer Biology

Selective Elimination of Osteosarcoma Cell Lines with Short Telomeres by ATR Inhibitors

T. Goncalves, G. Zoumpoulidou, C. Alvarez-Mendoza, L. C. Collopy, S. J. Strauss, S. Mittnacht, K. Tomita

This study identifies that osteosarcoma cell lines with short telomeres are selectively sensitive to ATR inhibitors, suggesting telomere length as a predictor of drug response.

bioRxiv · Aug 18, 2020Cancer Biology

Signalling involving MET and FAK supports cell division independent of the activity of the cell cycle-regulating CDK4/6 kinases

C. Zhang, S. R. Stockwell, M. Elbanna, R. Ketteler, J. Freeman, B. Al-Lazikani, S. Eccles, A. De Haven Brandon, F. Raynaud, A. Hayes, P. A. Clarke, P. Workman, S. Mittnacht

This study shows that MET/FAK signaling can activate CDK2 independently of CDK4/6, leading to cell division, and suggests targeting MET/FAK could enhance CDK4/6 inhibitor therapies.

bioRxiv · Apr 8, 2019Cancer Biology