RNaseH2 inhibition potentiates temozolomide response in patient derived glioblastoma cells.

ABSTRACT: Glioblastoma (GBM) is the most common and lethal form of primary brain tumor, characterized by poor prognosis and limited treatment options, with a median survival of only 12 to 15 months post-diagnosis. Despite standard therapeutic protocols involving temozolomide (TMZ) and radiotherapy, effective treatment is challenging, underscoring the need to explore alternative therapeutic strategies. One promising approach is the inhibition of DNA damage response (DDR) pathways. RNaseH2, a key enzyme involved in ribonucleotide excision repair (RER), plays a critical role in maintaining genomic stability by removing ribonucleotides misincorporated into DNA. Thus, inhibition of RNaseH2 may enhance tumor mutational burden (TMB) and potentially transform immunogenically "cold" tumors into immunogenical

SUBMITTER: Kissova M 

PROVIDER: S-EPMC12644484 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature