Table 1. Selinexor inhibits the steady state levels of gene products that regulate DNA damage repar of different mechanisms.

	Type of damage	Repair	Indication
Cisplatin	Alkylating agent cross links and induces bulky lesions	Nucleotide excision repair &Homologous recombination	Carcinomas, sarcomas, lymphomas, bladder cancer, cervical cancer and germ cell tumors [21]
Gemcitabine	Antimetabolite incorporates into DNA	Homologous recombination	Pancreatic, breast, ovarian, bladder and non-small cell lung cancer [22]
Doxorubicin & Idarubicin	Anthracyclines inhibit topo II and inhibit transcription, resulting in DSBs	Homologues recombination and non-homologous end joining	Leukemias, lymphomas, breast, stomach, uterine, ovarian, bladder and lung cancer [23]
Docetaxel	Inhibits microtubule dynamics, which disrupts DDR protein trafficking resulting in SSB	Base Excision Repair and Mismatch Repair	Breast, head and, stomach, prostate and non-small cell lung cancer [24]

HT1080 fibrosarcoma cells were treated with 0 (control), 100 or 1000 nM selinexor for 24 hours. Real-Time PCR gene expression assay demonstrates that selinexor inhibits DNA repair protein gene expression of several functional groups: Checkpoint (early response), recombination repair, base excision repair, nucleotide excision repair, and mismatch DNA repair mechanism.