In the January Editor's Choice article, Eric G. Thompson and co-authors show BRCA1 protects cells from error-prone repair of double-strand breaks by suppressing microhomology-mediated end joining and inhibiting mutagenesis during non-homologous end joining.
Hanssen-Bauer and colleagues developed a model including three modes of base excision, according to which three distinct complexes form through recruitment of different base excision repair proteins onto an XRCC1 core complex.
This work by Hernández et al. compared the benchmark dose that caused a 10% increase in endpoint response for in vivo genotoxicity and organ-matched carcinogenicity, and demonstrated a correlation between the endpoints.
The research article by Drs. McKinzie and Parsons is unique, in that it directly measures induction of a mutation with established importance in the azoxymethane rat colon cancer model (K-Ras codon 12 GAT mutation) only one week after exposure.