Results 81 to 90 of about 112,380 (305)
PARP inhibitors in ovarian cancer [PDF]
Cancer Treatment Reviews, 2019 Poly-ADP-ribosepolymerase inhibitors (PARPis) are the most active and interesting therapies approved for the treatment of epithelial ovarian cancer. They have changed the clinical management of a disease characterized, in almost half of cases, by extreme genetic complexity and alteration of DNA damage repair pathways, particularly homologous ...
Franzese, Elisena +9 more
openaire +3 more sources
Molecular Oncology, EarlyView.We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu +10 more
wiley +1 more source
PARP Inhibitors for Chemoprevention—Reply [PDF]
Cancer Prevention Research, 2014 We thank Brody and colleagues ([1][1]) for their thoughtful letter that raised three major issues about PARP inhibitors for chemoprevention: (i) long-term toxicity, (ii) secondary tumors, and (iii) drug resistance.
Ciric, To +2 more
openaire +2 more sources
PARP inhibitors induce a senescence phenotype in non‐small cell lung carcinoma cell lines
FEBS Open Bio, EarlyView.Talazoparib is the most potent inducer of senescence among different PARP1 inhibitors in human NSCLC cells. In the absence of PARP, no senescence phenotype was observed, demonstrating that PARP1 is necessary for the induction of senescence by this inhibitor.
Camille Huart +7 more
wiley +1 more source
Posttranscriptional regulation of PARG mRNA by HuR facilitates DNA repair and resistance to PARP inhibitors [PDF]
, 2017 The majority of pancreatic ductal adenocarcinomas (PDAC) rely on the mRNA stability factor HuR (ELAV-L1) to drive cancer growth and progression. Here, we show that CRISPR-Cas9–mediated silencing of the HuR locus increases the relative sensitivity of PDAC
Brody, Jonathan R. +17 more
core +1 more source
FEBS Open Bio, EarlyView.Drugs previously repurposed to target blood cancers reduced neuroblastoma and glioblastoma cell growth and viability. However, their levels of anticancer activity were different and their clinical application may be problematic due to side effects at effective doses.
Abhishek Kharawatkar +4 more
wiley +1 more source
Advances in the use of PARP inhibitor therapy for breast cancer
Drugs in Context, 2018 Poly-ADP-ribose polymerase 1 (PARP-1) and PARP-2 are DNA damage sensors that are most active during S-phase of the cell cycle and that have wider-reaching roles in DNA repair than originally described.
Kelly E McCann, Sara A Hurvitz
doaj +1 more source
Antitumor activity of the ERK inhibitor SCH772984 [corrected] against BRAF mutant, NRAS mutant and wild-type melanoma. [PDF]
, 2014 BackgroundIn melanoma, dysregulation of the MAPK pathway, usually via BRAF(V600) or NRAS(Q61) somatic mutations, leads to constitutive ERK signaling.
Atefi, Mohammad S +13 more
core +1 more source
Exposure to the complement C5b-9 complex sensitizes 661W photoreceptor cells to both apoptosis and necroptosis. [PDF]
, 2015 The loss of photoreceptors is the defining characteristic of many retinal degenerative diseases, but the mechanisms that regulate photoreceptor cell death are not fully understood.
Francesca Cordeiro, M +5 more
core +1 more source
PARP Inhibitors as P-glyoprotein Substrates [PDF]
Journal of Pharmaceutical Sciences, 2014 The cytotoxicity of PARP inhibitors olaparib, veliparib, and CEP-8983 were investigated in two P-glycoprotein (P-gp) overexpressing drug-resistant cell models (IGROVCDDP and KB-8-5-11). IGROVCDDP and KB-8-5-11 were both resistant to olaparib and resistance was reversible with the P-gp inhibitors elacridar, zosuquidar, and valspodar.
Lawlor, Denise +6 more
openaire +2 more sources