Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Interesting targets to overcome these cancer defense mechanisms are: PARP, DNA-PK, PI3K, ATM, ATR, CHK1/2, and WEE1 inhibitors.
|
29113422 |
2017 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
PARP inhibitors represent the most advanced clinical agents targeting specifically DNA repair mechanisms in cancer therapy.
|
23436410 |
2013 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Hence, the efficacy of PARP inhibitors in cancer therapy has been investigated and has progressed from the laboratory to clinics, with olaparib having already been approved by the US FDA for ovarian cancer treatment.
|
27995810 |
2017 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Several pharmacological inhibitors of PARP moved toward clinical testing for a variety of indications, including cardioprotection and malignant tumors, and in late 2014, olaparib became the first PARP inhibitor approved for human use for the therapy of ovarian cancer.
|
28695500 |
2017 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Exploiting interconnected synthetic lethal interactions between PARP inhibition and cancer cell reversible senescence.
|
31186408 |
2019 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Targeting of these pathways, especially through PARP inhibition, is now being exploited therapeutically to effect significant clinical responses in subsets of individuals, particularly in patients with ovarian cancer or prostate cancer, including cancers with a marked metastatic burden.
|
27169997 |
2016 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
For the time being, however, the current literature suggests that a viable PARP inhibitorchemotherapy hybrid targeting HR deficient cancers could be well on its way very soon.
|
28699513 |
2018 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Although PARP inhibitors may offer a therapeutic option for selected malignancies, the long-term effects of these agents have not yet been defined.
|
21424107 |
2011 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
RAD51 Mediates Resistance of Cancer Stem Cells to PARP Inhibition in Triple-Negative Breast Cancer.
|
28034904 |
2017 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Targeting DNA Repair in Cancer: Beyond PARP Inhibitors.
|
28003236 |
2017 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Combination with BETi could greatly expand the utility of PARP inhibition to patients with HR-proficient cancer.
|
28747513 |
2017 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In vitro, GV markedly induced cancer cell death and apoptotic marker PARP cleavage in wtp53-carrying cells.
|
24535435 |
2014 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The combined use of PI3K inhibitor BKM120 and PARP inhibitor Olaparib may be effective in ovarian cancers with a broader spectrum of cancer-associated genetic alterations but not limited to those with mutant PIK3CA or BRCA genes.
|
27426307 |
2016 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In conclusion, PBD-based ADC alone or in combination with a PARP inhibitor may have improved therapeutic window in patients with cancer carrying <i>BRCA</i> mutations.
|
30352801 |
2019 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
PARP Inhibitors for Cancer Therapy.
|
28388401 |
2017 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
FUND: This work was supported by grants from the National Science Centre, Poland (2013/09/N/NZ5/01831 to DP-T; 2012/05/B/NZ5/01867 to MC), Academy of Finland (254366 to NAR), Moikoinen Cancer Research Foundation (to NAR) and EU PARP Cluster grant (UDA-POIG.05.01.00-005/12-00/NCREMFP to SW).
|
31466918 |
2019 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Further investigation of N-MYC-regulated DDR gene targets and the biological and clinical significance of MYCN-PARP-DDR signaling will more fully elucidate the importance of the MYCN-PARP-DDR signaling pathway in the development and maintenance of NEPC.<i>Clin Cancer Res; 24(3); 696-707.©2017 AACR</i>.
|
29138344 |
2018 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The PARP inhibitor olaparib has recently been approved for human use for the therapy of cancer.
|
28146604 |
2018 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Targeting dePARylation selectively suppresses DNA repair-defective and PARP inhibitor-resistant malignancies.
|
30989114 |
2019 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The DNA-PK inhibitor, NU7441, induced resistance to rucaparib (<i>P</i> = 0.014) and HR function recovery in a BRCA1-defective cell line.<b>Conclusions:</b> This study has shown that NHEJ is defective in 40% of ovarian cancers, which is independent of HR function and associated with resistance to PARP inhibitors in <i>ex vivo</i> primary cultures.<i>Clin Cancer Res; 23(8); 2050-60.©2016 AACR</i>.
|
27702817 |
2017 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In this narrative review we discuss recent findings on the involvement of PARP family members in cancer stem cell biology and the benefit of their inhibition.
|
31202733 |
2019 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Normal cells can tolerate the DNA damage generated by PARP inhibition because of an efficient homologous recombination mechanism (HR); in contrast, cancer cells with a deficient HR are unable to manage the DSBs and appear especially sensitive to the PARP inhibitors (PARPi) effects.
|
27884198 |
2016 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
PARP inhibitors show promise as combination and single agents in cancer chemotherapy.
|
23193155 |
2013 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
New research shows that DNA polymerase θ is a key player in PARP-mediated DNA damage repair and essential for the survival of cancer cells where homologous recombination is compromised.
|
25851856 |
2015 |
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In this issue of Cancer Cell, Fang and colleagues (Fang et al., 2019) propose that sequential inhibitions of PARP and DNA damage checkpoint considerably widen the therapeutic window.
|
31185206 |
2019 |