https://www.selleckchem.com/
Mechanistically, we found ATR and PARP inhibitor treatment induces premature mitotic entry, which is significantly elevated in the setting of IDH1/2-mutations. These data highlight the potential efficacy of targeting HR defects in IDH1/2-mutant cancers and support the development of this combination in future clinical trials.Cancer evolves through the accumulation of somatic mutations over time. Although several methods have been developed to characterize mutational processes in cancers, these have not been specifically designed to identify mutational patte
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