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Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase
TLDR
It is proposed that, in the absence of PARP1, spontaneous single-strand breaks collapse replication forks and trigger homologous recombination for repair and exploited in order to kill BRCA2-deficient tumours by PARP inhibition alone.
Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase
TLDR
This corrects the article to show that the method used to derive the H2O2 “spatially aggregating force” is based on a two-step process, not a single step, like in the previous version of this paper.
PARP is activated at stalled forks to mediate Mre11‐dependent replication restart and recombination
TLDR
Together, the data suggest that PARP1 and PARP2 detect disrupted replication forks and attract Mre11 for end processing that is required for subsequent recombination repair and restart of replication forks.
Spontaneous Homologous Recombination Is Induced by Collapsed Replication Forks That Are Caused by Endogenous DNA Single-Strand Breaks
TLDR
It is suggested that a first homologous recombination event frequently triggers a second event at the same locus in mammalian cells.
Distinct microRNA alterations characterize high- and low-grade bladder cancer.
TLDR
It is found that altered microRNA expression is common in U CC and occurs early in tumorogenesis, and distinct microRNA alterations characterize UCC and target genes in a pathway-specific manner.
Inhibition of poly (ADP-ribose) polymerase activates ATM which is required for subsequent homologous recombination repair
TLDR
It is suggested that ATM is activated by PARP inhibitor-induced collapsed replication forks and may function upstream of HRR in the repair of certain types of double-strand breaks (DSBs) in non-homologous end joining (NHEJ).
Poly(ADP-ribose) Polymerase (PARP-1) in Homologous Recombination and as a Target for Cancer Therapy
TLDR
Although PARP-1 appears not to be required for homologous recombination itself, it regulates the process through its involvement in the repair of DNA single-strand breaks (SSBs), which triggers homological recombination for replication restart.
Critical research gaps and translational priorities for the successful prevention and treatment of breast cancer
TLDR
With resources to conduct further high-quality targeted research focusing on the gaps identified, increased knowledge translating into improved clinical care should be achievable within five years.
Poly(ADP-ribose) polymerase is hyperactivated in homologous recombination-defective cells.
TLDR
It is reported that PARP inhibitor-resistant BRCA2-mutant cells revert back to normal levels of PARP activity, and it is speculated that the reason for the sensitivity of HR-defective cells to PARP inhibitors is related to the hyperactivated PARP1 in these cells.
The ERCC1/XPF endonuclease is required for completion of homologous recombination at DNA replication forks stalled by inter-strand cross-links
TLDR
It is reported that mitomycin C-induced lesions inhibit replication fork elongation and suggested that ERCC1–XPF plays a role in completion of HR in ICL repair, and no additional sensitivity to cisplatin by siRNA co-depletion of XRCC3 and ER CC1 is found, showing that the two proteins act on the same pathway to promote survival.
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