Rachel Brough

Global signatures of Ribonucleotide Excision Repair deficiency and its therapeutic vulnerabilities

This study identifies RER deficiency as a new DNA repair defect in cancer, detectable through mutational signatures and linked to therapeutic vulnerabilities.

The FANCM-RMI1/2 complex promotes genomic instability and PARP inhibitor sensitivity in BRCA2-deficicient cells.

This study identifies FANCM-RMI1/2 as a driver of PARP inhibitor sensitivity in BRCA2-deficient cells, revealing distinct adaptation mechanisms between BRCA1 and BRCA2 loss.

Mutational and functional heterogeneity of homology-directed repair deficiency and clinical implications

The paper shows HRd is a continuum with functional and mutational heterogeneity, highlighting the need for refined molecular classification for precision interventions.

Reversion mutations define minimal BRCA1/2 requirements for therapy resistance

The paper identifies BRCA1/2 reversion mutations associated with drug resistance in cancer patients and highlights key domains critical for resistance.

LOX inhibition disrupts a collagen-integrin-MYC axis as a translatable targeting strategy in invasive lobular carcinoma

LOX inhibition disrupts a collagen-integrin-MYC axis in ILC, halting tumor growth and metastasis with minimal toxicity, offering a new therapeutic strategy.

CDK12 Loss Promotes Prostate Cancer Development While Exposing Vulnerabilities to Paralog-Based Synthetic Lethality

This study shows CDK12 loss drives prostate cancer development and identifies CDK13 as a therapeutic target through paralog-based synthetic lethality in CDK12-mutant tumors.