Cancer cells lacking BRCA1 or BRCA2 must adapt to proliferate despite pervasive genomic instability. To delineate BRCA1- and BRCA2-specific adaptation landscapes, we developed an isogenic screening platform enabling acute depletion of either protein. Genetic interaction profiling revealed hundreds of genes with shared,...
François Dossin, Mikaël Attia, Fabricio Montero-Zúñiga et al.· Molecules and Cells· 0 citations
Although mitotic cells normally suppress the expression of proteins involved in meiosis, a series of meiotic recombination proteins are commonly expressed in cancers, outside of their normal context. Here we review mechanistic and genomic evidence linking meiotic recombination proteins to cancer, focussing on HORMAD1,...
V. Amodeo, S. Pettitt, A. Tutt et al.· DNA Repair· 0 citations
Most Triple Negative Breast Cancers (TNBCs) are p53 mutant high-grade invasive ductal carcinomas with a basal-like transcriptional programme. A large proportion of TNBCs also have mutation signatures indicating defective homologous recombination (HR) DNA repair. While HR deficiency is mutagenic and oncogenic, it can al...
V. Amodeo, D. Weekes, Nicolae Balan et al.· Nature Communications· 0 citations
It is reported that DDIAS is a DNA-binding effector of the CIP2A pathway in human cells and proposed that DDIAS defines a mitotic DNA repair system downstream of CIP2A that mitigates the threat of mitotic ssDNA for genome integrity.
Yibo Xue, Faisal Bin Rashed, Daniel Y. L. Mao et al.· Molecules and Cells· 1 citation
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.
