Massimo Lopes

This study identifies FANCM-RMI1/2 as a driver of PARP inhibitor sensitivity in BRCA2-deficient cells, revealing distinct adaptation mechanisms between BRCA1 and BRCA2 loss.

This paper identifies a distinct HCC subgroup defined by high regeneration-associated stress, showing vulnerability to ATR inhibitors and proposing LIVRESS as a biomarker for treatment stratification.

This study identifies replication fork plasticity as a key determinant of therapy response in AML, showing that PrimPol mediates resistance to PARPi and araC.

This study shows that Lamin A/C modulates replication fork restart under stress by affecting H3K9me3 and PAR levels, impacting chromosome stability and chemotherapy response.

This study develops an experimental system to analyze GAA repeat expansions and replication fork stalling in human cells, finding that repeat expansions depend on proteins involved in replication fork stalling and restart.

This study identifies MDC1's role in replication fork restart and shows its loss leads to chemoresistance in BRCA1/2-deficient mammary tumors.

This study identifies PrimPol as a key player in ICL traverse, showing its primase activity is required for DNA damage tolerance and that its absence increases sensitivity to ICL-inducing drugs.