Results 51 to 60 of about 43,499 (244)
Cisplatin resistance coupled to enhanced sensitivity to metabolic interventions
Molecular & Cellular Oncology, 2018 Specific metabolic alterations have recently been observed in cisplatin-resistant cancers. As a result, cisplatin resistance can be overcome by co-administration of pyridoxine, and cisplatin-resistant cancer cells become exquisitely sensitive to killing ...
Maria Castedo +2 more
doaj +1 more source
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
Molecular 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
PARP Inhibitors: Clinical Relevance, Mechanisms of Action and Tumor Resistance
Frontiers in Cell and Developmental Biology, 2020 The Poly (ADP-ribose) polymerase (PARP) family has many essential functions in cellular processes, including the regulation of transcription, apoptosis and the DNA damage response.
Maddison Rose +5 more
doaj +1 more source
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
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
ToxicsUbiquitin-specific protease 1 (USP1) is an emerging target for poly(ADP-ribose) polymerase 1 (PARP1) inhibitor-resistant and BRCA1/BRCA2 mutant tumors.
Stefan M. Leonard +3 more
doaj +1 more source
Loss of amplified genes by poly(ADP-ribose) polymerase inhibitors.
Environmental Health Perspectives, 1991 A poly(ADP-ribose) polymerase inhibitor, benzamide (BA), was found to induce flat revertants of NIH 3T3 cells that had been transformed by human Ha-ras, rat Ki-ras, rat c-raf, and human ret-II. These genes had been amplified in original transformants, but they were completely eliminated by BA.
M, Nagao +4 more
openaire +2 more sources
Chromosomal Instability Drives Glioblastoma Heterogeneity and Therapeutic Opportunities
Advanced Science, EarlyView.ABSTRACT Glioblastoma, the most aggressive and lethal form of brain cancer, is defined by profound genomic instability, with Chromosomal Instability (CIN) playing a central role in driving tumor progression, therapy resistance, and poor prognosis. CIN is characterized by numerical and structural alterations, is driven by mechanisms such as mitotic ...
Amarnath Pal +3 more
wiley +1 more source
TDP‐43 Aggregation: The Healthy‐Toxic Balance of the Prion‐Like Domain
Advanced Science, EarlyView.TDP‐43 function relies on a delicate balance between reversible phase‐separated states and irreversible aggregation. Under physiological conditions, TDP‐43 forms dynamic droplets and oligomers that support normal cellular functions. In pathological contexts, this balance shifts toward aberrant aggregation, leading to toxic species.
Luca Zangrando +2 more
wiley +1 more source
Advanced Science, EarlyView.This study uncovers a metabolic‐epigenetic axis licensing zygotic genome activation (ZGA) in mouse embryos. A developmental decline in NAD+ levels activates PARP7, which mono‐ADP‐ribosylates and stabilizes UHRF1. This modification promotes the establishment of permissive histone acetylation marks, thereby facilitating timely ZGA.
Guangyi Cao +13 more
wiley +1 more source