Professor Helen E. Bryant — DNA replication & repair

DNA Replication & Repair Group

University of Sheffield

Welcome to our lab

From replication stress to targeted cancer therapy

We decode how cells respond to replication perturbation, translate that knowledge into predictive biomarkers and exploit vulnerabilities for therapeutic benefit — including targeted inhibitors and photo‑activated agents.

Read our research Selected publications

Principal Investigator

Professor Helen E. Bryant

Professor of Cancer Therapeutics

Professor Bryant is an internationally recognised genome biologist whose work contributed to the preclinical foundation for PARP‑inhibitor therapy and continues to translate DNA repair biology into new therapeutic strategies.

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Programmes

Four research programmes

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Replication-stress features associated with ATR-inhibitor sensitivity in neuroblastoma models.

Replication stress and fork stability

How do cells protect and restart stalled replication forks, and which vulnerabilities in tumour cells can be exploited therapeutically?

Selective sensitivity of DNA-damage-response-deficient cells to PARG inhibition.

PARP and PARG biology in synthetic lethality

How can defects in homologous recombination and related DNA-damage responses be exploited with PARP- and PARG-directed therapies?

Preclinical evaluation of ATM inhibition with radium-223 in prostate-cancer bone-metastasis models.

Checkpoint modulation and radiosensitisation

Can checkpoint and DNA-damage-response inhibitors improve tumour control with radiotherapy and radiopharmaceutical treatments?

Visible-light phototoxicity of a photostable iridium(III) photosensitiser in cancer cells and three-dimensional models.

Photoactivated therapeutics and chemical biology

Can visible-light-activated metal complexes deliver spatially controlled cancer-cell killing with limited dark toxicity?

Selected publications

Recent and defining work

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2005

Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase

Nature

↗2005

Poly(ADP-ribose) polymerase (PARP-1) in homologous recombination and as a target for cancer therapy

Cell Cycle

↗2009

PARP is activated at stalled forks to mediate Mre11-dependent replication restart and recombination

The EMBO Journal

↗2017

Specific killing of DNA damage-response deficient cells with inhibitors of poly(ADP-ribose) glycohydrolase

DNA Repair

↗2020

Poly(ADP-Ribose) Glycohydrolase (PARG) vs. Poly(ADP-Ribose) Polymerase (PARP): function in genome maintenance and relevance of inhibitors for anti-cancer therapy

Frontiers in Molecular Biosciences

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