|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In summary, our data support the potential use of PARP inhibitors in NSCLC with HR deficiency.
|
31753490 |
2020 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In the present study, we further investigated the antitumor activities of KJ-28d in <i>BRCA</i>-proficient non-small cell lung cancer (NSCLC) cells to expand the use of PARP inhibitors.
|
31795418 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
PARP inhibition enhances tumor cell-intrinsic immunity in ERCC1-deficient non-small cell lung cancer.
|
30589644 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
NSCLC RANBP9 KO cells were also more sensitive than control cells to the PARP inhibitor olaparib alone and in combination with cisplatin, due to defective ATM-dependent and hyper-activated PARP-dependent DDR.
|
30076413 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Whereas both veliparib, a PARP inhibitor that does not efficiently trap PARP1 to chromatin, and PARP1 depletion radiosensitized NSCLC cells as effectively as olaparib, which does efficiently trap PARP, only olaparib potentiated AZD1775-mediated radiosensitization.
|
29133592 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Smoking History Predicts Sensitivity to PARP Inhibitor Veliparib in Patients with Advanced Non-Small Cell Lung Cancer.
|
28461256 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The combination of the PARP inhibitor olaparib and rapamycin synergistically inhibited cell proliferation in non-small cell lung cancer (NSCLC) cells, and even in triple negative breast cancer (TNBC) cells with BRCA1 mutations.
|
29152062 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In conclusion, the reductive Apaf-1 regulated by miR-484 accelerated the NSCLC cell progression associated with the inhibition of apoptosis via down-regulating Caspase-3 and PARP cleavage.
|
28982084 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Triptolide reduced the viability of five non-small cell lung cancer (NSCLC) cells, the proliferation and self-renewal of pulmospheres, and levels of HA synthase 2 (HAS2), HAS3, HA, CD44, RHAMM, EGFR, Akt and ERK, but increased the cleavage of caspase 3 and PARP.
|
28460475 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
APR-246 (PRIMA-1(MET)) strongly synergizes with AZD2281 (olaparib) induced PARP inhibition to induce apoptosis in non-small cell lung cancer cell lines.
|
26975633 |
2016 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
CCDC6 could represent a predictive biomarker of resistance to conventional single mode therapy and yield insight on tumor sensitivity to PARP inhibitors in NSCLC.
|
25302833 |
2015 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
A deeper understanding of the DNA damage response in lung malignancies, and particularly a clarification of the crosstalk between DNA repair functionality and genetic stability, is the key to optimize the development of PARP inhibitors in the setting of NSCLC.
|
24191958 |
2014 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
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.
|
23275151 |
2013 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Collectively, our results indicate that CDDP can be advantageously combined with PARP inhibitors to kill several NSCLC cell lines, independently from their p53 status.
|
23428903 |
2013 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Taken together, the existence of BRCA1-immunodeficient NSCLC suggests that this molecular subgroup could be effectively targeted by PARP inhibitors in the clinic and that PARP inhibitors could be used for the treatment of BRCA1-immunodeficient, platinum-resistant tumours.
|
21706479 |
2011 |