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. 2019 Mar 30;8(4):435. doi: 10.3390/jcm8040435
aNHEJ alternative non-homologous end-joining
BER base excision repair
BID bis in die, twice a day
BRCA1/2 breast cancer type 1/type 2 susceptibility protein
CNA copy number alterations
CAT catalytic domain (of PARP-1)
CBR clinical benefit rate
CGH comparative genomic hybridization
CR complete response
DLT dose-limiting toxicities
DNMTi DNA methyltransferase inhibitor
DSB double-strand break
EMI1 early mitotic inhibitor 1
ER estrogen receptor
EZH2 enhancer of zeste homolog 2
gBRCAm germline BRCA mutation-associated
HD helical domain
HER2 human epidermal growth factor receptor 2
HRD homologous recombination deficiency/homologous recombination-deficient
HR hormone receptor
HRR homologous recombination repair
IRIF ionizing radiation induced foci
IV intravenous
LOH loss of heterozygosity
LST large-scale state transitions
miRNA micro RNA
NAD+ nicotinamide adenine dinucleotide
NHEJ non-homologous end-joining
ORR objective response rate
PARP poly (ADP-ribose) polymerase
PARPi poly (ADP-ribose) polymerase inhibitor
pCR pathological complete response
PCT physician’s choice of chemotherapy
PFS progression-free survival
PO per os, by mouth
PR progesterone receptor
PRC2 polycomb repressive complex 2
PRR partial response rate
QD quaque die, once a day
RER ribonucleotide excision repair
ROS reactive oxygen species
RP2D recommended phase 2 dose
SD stable disease
SNP single-nucleotide polymorphism
SSA single-strand annealing
TAI telomeric allelic imbalance
TNBC triple negative breast cancer
TOP1 topoisomerase 1