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Palabras clave – provistas por la editorial

MDS; PARP inhibitors; olaparib; hematopoietic differentiation; PARP1; AML; poly-ADP-ribose polymerase 1 (PARP1); brahma-related gene 1 (BRG1); histone acetyltransferase p300 (EP300); gene transcription; cancer cell; head and neck squamous cell carcinoma; CAL27; SCC90; p60/p150 CAF-1 subunits; DNA repair; homologous recombination; biomarkers; personalized treatment; UVB; PARP; mitochondria; metabolism; biogenesis; autophagy; carcinogenesis; transcription; PARylation; DNA damage; transcription silencing; carryover effect; TOP1 activity; TDP1; irinotecan; immunomodulation; tumor microenvironment; trapping; cancer therapeutic strategy; arginine-specific mono-ADP-ribosylation; bacterial toxin; cholera toxin; ART1; ARH1; tumorigenesis; loss of heterozygosity; membrane repair; gender bias; Syk; EGFR; squamous cell carcinoma; PARP-Akt interplay; PI3K; mTOR; cytoprotection; apoptosis resistance; oxidative stress; mitochondrial protection; drug development; synthetic lethality; clinical trials; ADP-ribosylation; cancer; macrodomain; ADP-ribosyl hydrolase; ARTD; MACROD1; MACROD2; TARG1; ATM; ATR; PARP inhibitor; prostate cancer; pancreatic cancer; lung cancer; Tumor microenvironment; PARPs; hypoxia; CHK1; replication stress; homologous recombination DNA repair; cell cycle; cytotoxicity; PARP Inhibitors; beta-lapachone; NQO1; PARG; NAMPT; cancer therapeutics; cMET; poly (ADP-ribose) glycohydrolase; radiosensitization; poly (ADP-ribose) polymerase; ES cells; poly (ADP-ribose) polymerase inhibitors (PARPi); ataxia telangiectasia and Rad3 related inhibitors (ATRi); cell cycle checkpoints; NAD+; NMNAT1; cisplatin; chemotherapy; apoptosis; osteosarcoma; DNA damage response; immunotherapy; immune checkpoint inhibitor; PD-1; PD-L1; CTLA-4; combination therapy; solid tumors; the PARP inhibitor PJ34; distorted mitotic spindles; exclusive eradication of human cancer cells; nucleolus; poly(ADP-ribosyl)ation; ARTDs; n/a