Ubiquitination is an essential regulator of most, if not all, signalling pathways, and defects in
cellular signalling are central to cancer initiation, progression and, eventually, metastasis …

Ubiquitination is a reversible post-translational modification based on the chemical addition
of ubiquitin to proteins with regulatory effects on various signaling pathways. Ubiquitination …

In recent years, synthetic lethality has been recognized as a solid paradigm for anticancer
therapies. The discovery of a growing number of synthetic lethal targets has led to a …

DNA replication stress-induced fork arrest represents a significant threat to genomic
integrity. One major mechanism of replication restart involves repriming downstream of the …

DNA damage triggers cell signaling cascades that mediate repair. This signaling is
frequently dysregulated in cancers. The proteins that mediate this signaling are potential …

Defects in DNA repair pathways play a pivotal role in tumor evolution and resistance to
therapy. At the same time, they create vulnerabilities that render tumors dependent on the …

Recent studies suggest that PARP and POLQ inhibitors confer synthetic lethality in BRCA1-
deficient tumors by accumulation of single-stranded DNA (ssDNA) gaps at replication forks …

Translesion DNA synthesis (TLS) is a DNA damage tolerance pathway utilized by cells to
overcome lesions encountered throughout DNA replication. During replication stress, cancer …

PARP inhibitors (PARPi) represent a game-changing treatment for patients with ovarian
cancer with tumors deficient for the homologous recombination (HR) pathway treated with …

Motivation Synthetic lethality (SL) is a promising strategy for anticancer therapy, as inhibiting
SL partners of genes with cancer-specific mutations can selectively kill the cancer cells …