XRCC1 (X-Ray Repair Cross Complementing 1)

Advancements such as next-generation sequencing and immunogenetics, which identify the relationship between HPV variants and host immune genes that modulate disease susceptibility, vaccine responsiveness, and progression patterns across various genetic backgrounds. This review systematically integrates molecular mechanisms of HPV variant-induced oncogenesis and host genetic susceptibility with emphasis on population-based variability in addition to evidence culled from meta-analyses and GWAS data for immune regulation, DNA repair, as well as host single nucleotide polymorphisms in different populations and its implications for personalized prevention measures, screening, and vaccine response.

PARP inhibition with olaparib increased residual γH2AX/53BP1 foci post-irradiation in ERG+ cells, indicating enhanced radiosensitization...These findings suggest that ERG expression promotes dependency on PARP1-EJ, rendering ERG+ PCa more susceptible to PARP inhibition. Combining PARP inhibitors with RT may offer a tumor-selective radiosensitization for ERG+ PCa patients.

Using mouse embryonic stem cells, we showed that BRCA1-mediated homologous recombination promotes rDNA instability, the non-homologous end joining factor XRCC1, but not Ku, suppresses intra-cluster deletions, and ATM kinase preserves rDNA cluster stability. Together, these findings establish a platform and tools for studying rDNA instability in animal models relevant to aging and cancer research.

Although several DNA repair gene polymorphisms have been explored, findings remain inconsistent and limited by populations and SNPs studied. Larger, well-designed studies with standardized methodologies are needed to confirm these associations and identify genetic markers for predicting high-risk patients for CIO.

Eg5 inhibitors specifically bind to the Eg5 protein and disrupt mitosis, thereby improving the radiosensitivity of RCC by regulating the cell cycle. An Eg5 inhibitor combined with radiotherapy may represent an effective adjuvant therapy for RCC.

Finally, inhibition of the ATR regulators PRMT1 or PRMT5 synergizes with PARG inhibition, implicating replication-associated BER/SSBR and PARylation in the activation of the PRMT1/PRMT5/ATR axis. This study highlights the role of BER/SSBR in protecting the cell during S-phase to suppress PARylation-induced checkpoint activation, which may suggest a potential intervention strategy for PARG inhibitor-resistant tumors.

The DNA damage-responsive, 3q26-q29 amplicon-encoded lncRNA PARylator promotes PARP1‑mediated PARylation and SSB repair, thereby limiting DSB accumulation and supporting ESCC cell survival and resistance to DNA-damaging therapies. Targeting PARylator, alone or in combination with DNA-damaging agents, may represent a novel avenue for ESCC treatment.

Although XRCC1 and MTHFR polymorphisms have been extensively studied, their predictive utility remains inconclusive. Future research should prioritize large, multicenter prospective studies with standardized treatment and outcome definitions, and consider polygenic risk models or integrated multi-omic approaches.

FEN1 rs174538 A>G, FEN1 rs4246215 T>G, APEX1 rs3136817 T>C, and XRCC1 rs25487 C>T are associated with Wilms tumor susceptibility, which provides potential molecular markers for the early diagnosis of Wilms tumor.

Overall, the data suggest that XRCC1 Arg399Gln might be associated with increased CRC susceptibility, while Arg194Trp and Arg280His are not significantly associated.