Homologous recombination deficiency and ovarian cancer [PDF]
The discovery that PARP inhibitors block an essential pathway of DNA repair in cells harbouring a BRCA mutation has opened up a new therapeutic avenue for high-grade ovarian cancers.
Drew, Y, Kristeleit, RS, Ledermann, JA
core +1 more source
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
Posttranscriptional regulation of PARG mRNA by HuR facilitates DNA repair and resistance to PARP inhibitors [PDF]
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
Medical treatment of early stage and rare histological variants of epithelial ovarian cancer [PDF]
Epithelial ovarian cancer is often considered a single pathological entity, but increasing evidence suggests that it is rather a group of different neoplasms, each with unique pathological characteristics, molecular features, and clinical behaviours ...
Biglia, Nicoletta +6 more
core +3 more sources
Nanoparticle Formulations of Poly (ADP-ribose) Polymerase Inhibitors for Cancer Therapy
A number of poly(ADP-ribose) polymerase (PARP) inhibitors have been recently approved for clinical use in BRCA mutated and other cancers. However, off-target toxicity of PARP inhibitors and the emergence of drug resistance following prolonged ...
Bijay Singh +10 more
doaj +1 more source
Dual Inhibitors of PARPs and ROCKs [PDF]
Recent network and system biology analyses suggest that most complex diseases are regulated by robust and highly interconnected pathways that could be better modulated by small molecules binding to multiple biological targets. These pieces of evidence recently led to devote efforts on identifying single chemical entities that bind to two different ...
Albert A. Antolín, Jordi Mestres
openaire +5 more sources
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis +3 more
wiley +1 more source
BH3 mimetic ABT-737 sensitizes colorectal cancer cells to ixazomib through MCL-1 downregulation and autophagy inhibition. [PDF]
The proteasome inhibitor MLN9708 is an orally administered drug that is hydrolyzed into its active form, MLN2238 (ixazomib). Compared with Bortezomib, MLN2238 has a shorter proteasome dissociation half-life and a lower incidence and severity of ...
Barkhouse, Darryll +7 more
core +2 more sources
PARP inhibitors induce a senescence phenotype in non‐small cell lung carcinoma cell lines
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
The kinesin Eg5 inhibitor K858 induces apoptosis but also survivin-related chemoresistance in breast cancer cells [PDF]
Inhibitors of kinesin spindle protein Eg5 are characterized by pronounced antitumor activity. Our group has recently synthesized and screened a library of 1,3,4-thiadiazoline analogues with the pharmacophoric structure of K858, an Eg5 inhibitor.
CARRADORI, Simone +8 more
core +1 more source

