Results 231 to 240 of about 718,683 (284)

The mitochondrial translocation of phosphorylated EZH2 promotes PARP inhibitor resistance in BRCA1-deficient epithelial ovarian cancer. [PDF]

open access: yesCell Discov
Hu L   +15 more
europepmc   +1 more source

Emergence of BRCA Reversion Mutations in Prostate Cancer Prior to PARP Inhibitor Exposure: Clinical and Therapeutic Implications. [PDF]

open access: yesCancer Med
Lin DI   +11 more
europepmc   +1 more source

PARP inhibitor combination therapy

open access: yesCritical Reviews in Oncology/Hematology, 2016
In 2014, olaparib (Lynparza) became the first PARP (Poly(ADP-ribose) polymerase) inhibitor to be approved for the treatment of cancer. When used as single agents, PARP inhibitors can selectively target tumour cells with BRCA1 or BRCA2 tumour suppressor gene mutations through synthetic lethality.
Christopher Lord, Alan Ashworth
exaly   +5 more sources

The Vasoactivity of PARP Inhibitors

2015
PARP-inhibition has proven to be an attractive therapeutic approach in cancer whereby the effectiveness of DNA-damaging therapy can be enhanced by inhibiting the PARP-mediated DNA-repair process. Generally there is good concordance between enhanced therapeutic efficacy in vitro and that observed in vivo.
Williams, Kaye J., McCrudden, Cian M.
openaire   +2 more sources

PARP Inhibitors

Current Breast Cancer Reports, 2011
Poly (ADP-ribose) polymerase (PARP) is a novel therapeutic target in cancer. Preclinical studies demonstrate that PARP inhibitors selectively kill BRCA-deficient cells and potentiate the effects of DNA-damaging agents. There are several PARP inhibitors in clinical development, including olaparib, iniparib, veliparib, PF-01367338, and MK-4827.
Hongyan Liang, Antoinette R. Tan
openaire   +2 more sources

Tackling PARP inhibitor resistance

Trends in Cancer, 2021
Homologous recombination-deficient (HRD) tumours, including those harbouring mutations in the BRCA genes, are hypersensitive to treatment with inhibitors of poly(ADP-ribose) polymerase (PARPis). Despite high response rates, most HRD cancers ultimately develop resistance to PARPi treatment through reversion mutations or genetic/epigenetic alterations to
Fugger, Kasper   +3 more
openaire   +3 more sources

PARP inhibitors coming of age

Nature Reviews Clinical Oncology, 2020
The much anticipated results from two phase III studies evaluating the clinical efficacy of poly(ADP-ribose) polymerase (PARP) inhibition in patients with advanced-stage breast cancer harbouring a germline mutation in BRCA1/2 have established new therapeutic opportunities and yet, have left us with several ongoing questions.
Shani Paluch-Shimon, Fatima Cardoso
openaire   +2 more sources

PARP inhibitors.

IDrugs : the investigational drugs journal, 2005
Poly(ADP-ribose) polymerase (PARP) catalyzes the biochemical conversion of nicotinamide adenine dinucleotide (NAD+) to poly(ADP-ribose) and nicotinamide, which is a weak feedback inhibitor of the enzyme. Early designs of PARP inhibitors were primarily based on mimicking the structure of nicotinamide and resulted in the identification and widespread use
J H, Li, J, Zhang
openaire   +3 more sources

PARP Inhibitors in Prostate Cancer

Current Treatment Options in Oncology, 2017
The genomic landscape of metastatic prostate cancer (mPCa) reveals that up to 90% of patients harbor actionable mutations and >20% have somatic DNA repair gene defects (DRD). This provides the therapeutic rationale of PARP inhibition (PARPi) to achieve "synthetic lethality" in treating this fatal disease. Clinical trials with PARP inhibitors have shown
Praveen, Ramakrishnan Geethakumari   +3 more
openaire   +2 more sources

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