|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
<i>BRCA</i> Reversion Mutations in Circulating Tumor DNA Predict Primary and Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma.
|
30425037 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
<i>IDH</i>-Mutant Tumors Vulnerable to PARP Inhibition.
|
28228392 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Tumor BRCA Test for Patients with Epithelial Ovarian Cancer: The Role of Molecular Pathology in the Era of PARP Inhibitor Therapy.
|
31653094 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
PARP inhibitors) or that target tumor survival pathways, such as Akt inhibitors, glycolysis inhibitors or mTOR inhibitors, are of high interest.
|
19648052 |
2010 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
COL11A2 overexpression and BMP7 underexpression could collaborate to OS tumor growth, through its central role in bone remodeling process.
|
20225287 |
2010 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
PARP inhibitors (PARPi) for the treatment of BRCA1 or BRCA2 deficient tumours are currently the focus of seminal clinical trials exploiting the concept of synthetic lethality.
|
23165508 |
2013 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
PARP inhibitors have gained recent attention as promising therapeutic agents for the treatment of solid tumours including breast cancer (BC).
|
25528020 |
2015 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
PARP inhibitors target DNA repair and provide a second hit to BRCA mutated tumors, resulting in "synthetic lethality".
|
27282964 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
PARP inhibition is known to be an effective clinical strategy in BRCA mutant cancers, but PARP inhibition has not been applied to BRCA-proficient tumors.
|
29262321 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
PARP inhibitors (PARPi) are potentially effective therapeutic agents capable of inducing synthetic lethality in tumors with deficiencies in homologous recombination (HR)-mediated DNA repair such as those carrying BRCA1 mutations.
|
29592899 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
PARP inhibitors (PARPis) have been used to induce synthetic lethality in BRCA-deficient tumors in clinical trials with limited success.
|
29898385 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
PARP inhibition enhances tumor cell-intrinsic immunity in ERCC1-deficient non-small cell lung cancer.
|
30589644 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
After 30 day TQ and/or cisplatin treatment, we measured the following indices: tumor burden (ascites volume, number of peritoneal implants and mesenteric tumor mass); NF-κB reporter activity (luciferase assay); protein expression of the double-strand DNA break marker, pH2AX(ser139), the proliferation markers, Ki67/mib-1 and PCNA, and the apoptosis markers, cleaved caspase-3, cleaved PARP and Bax; and mRNA expression of NF-κB targets, TNF-α and IL-1β.
|
26215403 |
2015 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Apoptotic protein changes detected after exposure to wogonin included decreased XIAP and Mcl-1 expression, increased cleaved-PARP expression and increased release of AIF and cytochrome C. Western blot analysis showed that the activity of c-Myc/Skp2 and HDAC1/HDAC2 pathways, which play important roles in tumor progress, was decreased.
|
24265759 |
2013 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Based on its mechanism of action, PARP inhibitor therapy is expected to benefit mainly tumor cases with homologous recombination deficiency (HRD).
|
29917049 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Because many variants cannot be detected in DNA from blood, testing tumor DNA as the first step can double the identification rate of patients who stand to benefit most from PARP inhibitors.
|
31076742 |
2020 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
By identifying novel predictive biomarkers of tumour cell sensitivity to olaparib, it is possible that the utility of PARP inhibitors could be extended beyond this patient subgroup.
|
25883215 |
2015 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
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 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Cells positive for cleavage to active caspase-3 and 85 kDa PARP, and apoptosis were hardly observed in the tumors when they were treated with glycerol or CDDP alone.
|
15010879 |
2004 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
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 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Currently, inhibitors of immune tolerance and immune checkpoint inhibitors; PARP inhibitors; novel cytotoxic chemotherapies, such as trifluridine/tipiracil; and modifiers of the tumor microenvironment, such as pegylated hyaluronidase, are in clinical trials for the treatment of pancreatic cancer.
|
30681819 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
DEK significantly upregulated the expression levels of pro-apoptotic proteins such as cleaved caspase-3, cleaved caspase-9, cleaved PARP, p53, Bax, and tumor suppressor p21<sup>Cip1/Waf1</sup>, downregulated the levels of cell cycle regulating proteins such as cyclinD1, CDK2, and CDK4 and carcinogenic proteins such as EGFR and COX-2, and suppressed the activation of Akt.
|
28169543 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Downregulation of RAD51 by shRNA sensitized CSCs to PARP inhibition and reduced tumor growth.
|
28034904 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Embelin-treated mice showed significant inhibition in tumor growth which was associated with reduced expression of markers of cell proliferation (Ki67, PCNA and Bcl-2) and cell cycle (cyclin D1, CDK2, and CDK6), and induction of apoptosis (activation of caspase-3 and cleavage of PARP, and increased expression of Bax).
|
24694877 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Emerging data suggest that drugs that target poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP) enzymes may represent a novel and effective means of treating tumors with these DNA repair defects, including prostate cancers.
|
27188668 |
2016 |