The underlying mechanism for the PARP and BRCA synthetic lethality: Clearing up the misunderstandings

By Thomas Helleday. Molecular Oncology, 2011

830 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/e285c3c2783707a4126ed9cd2692752426a09b30

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. N. Almansour
2. J. R. Chapman
3. S. Boulton
4. F. Batista
5. Martin R. G. Taylor

In Oncology

1. N. Almansour
2. J. R. Chapman
3. S. Boulton

Citations in the corpus

• RIF1 Is Essential for 53BP1-Dependent Nonhomologous End Joining and Suppression of DNA Double-Strand Break Resection (2013, background): “BRCA1-deficient cells are hypersensitive to poly(ADP-ribose) polymerase (PARP) inhibitors (PARPi), which trigger the formation of replication-associated DNA damage that requires HR for its resolution (Bryant et al., 2005; Farmer et al., 2005; Helleday, 2011).”
• Playing the end game: DNA double-strand break repair pathway choice. (2012, background): “BRCA1- and BRCA2-defi- cient cells and tumors are intrinsically sensitive to inhibitors of poly(ADP-ribose) polymerase (PARPi), implicating such drugs as effective chemotherapeutic agents in the treatment of BRCA-associated cancers (Helleday, 2011).”
• Triple-Negative Breast Cancer: A Brief Review About Epidemiology, Risk Factors, Signaling Pathways, Treatment and Role of Artificial Intelligence (2022, background): “It has been observed that when PARP activity is affected, it blocks DNA polymerase ε for DNA damage repair (Helleday, 2011).”