Collectively, these data suggest that there is a synergistic relationship between PARP inhibition and low ERCC1 expression in NSCLC that could be exploited for novel therapeutic approaches in lung cancer therapy based on tumor ERCC1 expression.

XRCC1 Arg399Gln, PARP1 Va1762Ala and APE1 Asp148Glu SNPs in the base excision repair pathway may influence the prognosis of advanced non-small cell lung cancer patients following platinum-based chemotherapy

PARP hyperactivation is associated with cisplatin resistance in non-small cell lung carcinoma.

High PARP1 expression is associated with non-small cell lung cancer.

Niraparib (MK-4827), a novel poly(ADP-Ribose) polymerase inhibitor, radiosensitizes human lung and breast cancer cells.

The study found that PARP-1 rs3219073 C>G polymorphism is indeed associated with lung cancer susceptibility. The carriers of G alleles may have reduced risk of lung cancer, especially adenocarcinoma.

PARP1 expression was independently related to longer progression-free survival in limited-stage small cell lung cancer.

Non-small cell lung cancer patients with high intra-tumoral PARP1 activity had a poor prognosis.

these findings provide a foundation for the potential use of PARP1 inhibitors as a new treatment option for lung adenocarcinoma patients with elevated PARP1 expression.

Activation of the PI3K/mTOR pathway following PARP Inhibition in Small Cell lung cancer.

Overexpression of miR-335 decreased the expression of PARP-1 mRNA and protein, and NF-kappaB protein levels were correspondingly downregulated, thus regulating the chemo-radiosensitivity of small cell lung cancer cells.

this study identifies the importance of TDP1 as a novel determinant of response to CNDAC across various cancer types (especially non-small cell lung cancers), and demonstrates the differential involvement of BRCA2, PARP1, and TDP1 in the cellular responses to CNDAC, AraC, and CPT

PARP inhibition enhances tumor cell-intrinsic immunity in ERCC1-deficient non-small cell lung cancer.

Role of PARP1-mediated autophagy in EGFR-TKI resistance in non-small cell lung cancer.

Association of PARP1-specific polymorphisms and haplotypes with non-small cell lung cancer subtypes.

PARP-1 induces EMT in non-small cell lung carcinoma cells via modulating the transcription factors Smad4, p65 and ZEB1.

Data show reduced tumor burden through increased oxidative stress in lung adenocarcinoma cells of PARP-1 and PARP-2 knockout mice.