The endonuclease EEPD1 mediates synthetic lethality in RAD52-depleted BRCA1 mutant breast cancer cells.

Robert HromasHyun-Suk KimGurjit SidhuElizabeth WilliamsonAruna JaiswalTaylor A TotterdaleJocelyn NoleSuk-Hee LeeJac A NickoloffKimi Y Kong

Published in: Breast cancer research : BCR (2017)

This study indicates that the mechanism of synthetic lethality in RAD52-depleted BRCA1 mutant cancer cells depends on the endonuclease EEPD1. The data imply that EEPD1 cleavage of stressed replication forks may result in a toxic intermediate when replication fork repair cannot be completed.

Keyphrases

dna repair
dna damage
breast cancer cells
wild type
electronic health record
breast cancer risk
machine learning
big data
dna binding
transcription factor
artificial intelligence
data analysis