UNASSIGNED: There is a need to develop new, more efficient therapies for @entity135 ( @entity213 ) @entity1 . It is currently unclear whether defects in DNA repair genes play a role in HNSCCs' resistance to therapy. @entity12982 inhibitors (PARPi) were found to be "synthetic lethal" in @entity5 in @entity5345 /2 with impaired homologous recombination. Since @entity5 rarely have these particular mutations, there is considerable interest in finding alternative determinants of PARPi sensitivity. Effectiveness of combined irradiation and PARPi olaparib was evaluated in ten @entity213 cell lines, subdivided into HR-proficient and @entity942 cell lines using a GFP-based reporter assay. Both groups were equally sensitive to PARPi alone. Combined treatment revealed stronger synergistic interactions in the @entity942 group. Because HR is mainly active in S-Phase, replication processes were analyzed. A stronger impact of treatment on replication processes (p = 0.04) and an increased number of radial chromosomes (p = 0.003) were observed in the @entity942 group. We could show that radiosensitization by inhibition of @entity12982 strongly correlates with HR competence in a replication-dependent manner. Our observations indicate that @entity12982 inhibitors are promising candidates for enhancing the therapeutic ratio achieved by radiotherapy via disabling DNA replication processes in @entity942 HNSCCs.

@entity12982 inhibition radiosensitizes XXXX in homologous recombination by disabling the DNA replication fork elongation response.

@entity1 :: ('9606', 'Species') :: ['patients'] @entity135 :: ('MESH:D006258', 'Disease') :: ['head and neck cancer'] @entity5 :: ('MESH:D009369', 'Disease') :: ['cancers deficient', 'tumors'] @entity5345 :: ('672', 'Gene') :: ['BRCA1'] @entity12982 :: ('142', 'Gene') :: ['PARP1'] @entity942 :: ('MESH:D003677', 'Disease') :: ['HR-deficient'] @entity213 :: ('MESH:C535575', 'Disease') :: ['HNSCC']
@entity213 :: (MESH:C535575,Disease) :: ['HNSCC cells deficient']
