POLQ mediated end-joining promotes DNA damage tolerance in neuroblastoma.

ABSTRACT: Segmental chromosomal alterations, including 11q deletion and 17q gain, are the strongest predictors of pediatric neuroblastoma relapse. These alterations result from unbalanced translocations linked to erroneous DNA repair. Breakpoint sequence analysis suggests that these abnormalities arise through a nonhomologous end-joining mechanism, indicating a potential therapeutic opportunity. While the exact components driving this DNA end-joining process in neuroblastoma remain unknown, polymerase theta-mediated end-joining (TMEJ) has been implicated in other homologous recombination-deficient cancers. Our previous work demonstrated that high-risk neuroblastoma expresses elevated levels of TMEJ components, including DNA Ligase III and Ligase I, while downregulating classical NHEJ factors (DNA Li

SUBMITTER: Chukkapalli S 

PROVIDER: S-EPMC12177186 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature