Author

S. T. Durant

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

Frequent Co-Authors

J. V. Forment· 2 shared A. A. Sartori· 1 shared A. Barros· 1 shared A. Bradley· 1 shared A. Duarte· 1 shared A. Farooqi· 1 shared A. Hindle· 1 shared A. N. Kousholt· 1 shared

Activity by Year

2018-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 15 mutual co-author links

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2 shared papersCancer Biology

J. V. Forment

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

H2AX promotes replication fork degradation and chemosensitivity in BRCA-deficient tumours

D. Dibitetto, M. Liptay, F. Vivalda, E. Gogola, H. Dogan, M. G. Fernandez, A. Duarte, J. A. Schmid, S. T. Durant, J. V. Forment, I. Klebic, M. Siffert, R. de Brujin, A. N. Kousholt, N. A. Marti, , S. Rottenberg

This study identifies H2AX's role in promoting replication fork degradation and chemosensitivity in BRCA-deficient tumours, independent of its classical DNA damage signalling function.

bioRxiv · May 22, 2023Cancer Biology

ALT Neuroblastoma Chemoresistance due to ATM Activation by Telomere Dysfunction is Reversible with the ATM Inhibitor AZD0156

B. Koneru, A. Farooqi, T. H. Nguyen, W. H. Chen, A. Hindle, C. Eslinger, M. R. Makena, T. A. Burrow, J. Wilson, A. Smith, V. P. Reddy, E. Cadogan, S. T. Durant, C. P. Reynolds

This study shows that ATM activation due to telomere dysfunction causes chemoresistance in ALT neuroblastoma, which can be reversed by the ATM inhibitor AZD0156.

bioRxiv · Apr 6, 2021Cancer Biology

ATM orchestrates the DNA-damage response to counter toxic non-homologous end-joining at broken replication forks

G. Balmus, D. Pilger, J. Coates, M. Demir, M. Sczaniecka-Clift, A. Barros, M. Woods, B. Fu, F. Yang, E. Chen, M. Ostermaier, T. Stankovic, H. Ponstingl, M. Herzog, K. Yusa, , S. P. P. Jackson

The paper identifies how ATM counteracts toxic non-homologous end-joining at broken replication forks by showing that loss of NHEJ components or BRCA1-A complex confers resistance to DNA-damaging agents in ATM-deficient cells.

bioRxiv · May 24, 2018Cell Biology