Results 21 to 30 of about 45,197 (186)

Mechanisms of PARP inhibitor resistance in cancer and insights into the DNA damage response

open access: yesGenome Medicine, 2018
Editorial summary Inhibitors of poly(ADP-ribose) polymerase (PARPi) have entered the clinic for the treatment of patients with cancers that lack homology-directed DNA repair, but drug resistance remains a clinical hurdle.
Paola Francica, Sven Rottenberg
doaj   +1 more source

The Promise of Poly(ADP-Ribose) Polymerase (PARP) Inhibitors in Gliomas [PDF]

open access: yesJournal of Immunotherapy and Precision Oncology, 2020
Diffuse infiltrating gliomas are a clinically and molecularly heterogeneous group of tumors that are uniformly incurable. Despite our growing knowledge of genomic and epigenomic alterations in gliomas, standard treatments have not changed in the past 2 ...
Nazanin Majd   +3 more
doaj   +1 more source

Inputs and outputs of poly(ADP-ribosyl)ation: Relevance to oxidative stress

open access: yesRedox Biology, 2014
Oxidative stress can cause DNA breaks which induce activation of the DNA nick sensor enzyme poly(ADP-ribose) polymerase-1 (PARP-1), part of the 17 member PARP enzyme family.
Csaba Hegedűs, László Virág
doaj   +1 more source

Pan-cancer landscape of homologous recombination deficiency

open access: yesNature Communications, 2020
Cancers deficient in homologous recombination can benefit from treatment with poly ADP-ribose polymerase (PARP) inhibitors. Here, the authors generated a classifier that can predict homologous recombination deficiency from genomic data and suggest ...
Luan Nguyen   +3 more
doaj   +1 more source

Background-Quenched Aggregation-Induced Emission through Electrostatic Interactions for the Detection of Poly(ADP-ribose) Polymerase-1 Activity

open access: yesMolecules, 2023
Poly(ADP-ribose) polymerase-1 (PARP1) is a potential biomarker and therapeutic target for cancers that can catalyze the poly-ADP-ribosylation of nicotinamide adenine dinucleotide (NAD+) onto the acceptor proteins to form long poly(ADP-ribose) (PAR ...
Fengli Gao   +3 more
doaj   +1 more source

Poly(ADP-ribose) polymerase regulates transient receptor potential channel M2-dependent calpain activation in rd1 mouse retinal degeneration

open access: yesNeural Regeneration Research
Inherited retinal degeneration refers to untreatable blinding diseases characterized by progressive photoreceptor loss. Photoreceptor degeneration is often associated with an excessive activation of poly(ADP-ribose) polymerase and Ca2+-dependent calpain ...
Jie Yan   +9 more
doaj   +1 more source

Poly (ADP-Ribose) Polymerase Inhibitors: Talazoparib in Ovarian Cancer and Beyond

open access: yesDrugs in R&D, 2020
Genetic complexity and DNA damage repair defects are common in different cancer types and can induce tumor-specific vulnerabilities. Poly(ADP-ribose) polymerase (PARP) inhibitors exploit defects in the DNA repair pathway through synthetic lethality and ...
Stergios Boussios   +8 more
doaj   +1 more source

Phase I study of the PARP inhibitor talazoparib with radiation therapy for locally recurrent gynecologic cancers

open access: yesClinical and Translational Radiation Oncology, 2020
Summary: PARP inhibitors have been shown to radiosensitize tumor cells in both in vitro and in vivo studies. This is a phase I study that aims to determine the safety, tolerability, and maximally tolerated dose of talazoparib, a PARP inhibitor, when ...
David S. Lakomy   +3 more
doaj   +1 more source

NADP+ is an endogenous PARP inhibitor in DNA damage response and tumor suppression

open access: yesNature Communications, 2019
Cancer cells respond differently to inhibitors of Poly (ADP-ribose) polymerase. Here the authors reveal that ovarian cancer cells with higher cellular NADP+ levels are more sensitive to clinically relevant PARP1 inhibitors and show that NADP+ act as an ...
Chunjing Bian   +9 more
doaj   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
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

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