fig1

Figure 1. Gene transcription regulated by MYB, MYBL2, and MYB fusions (e.g., MYB-NFIB) plays a crucial role in the resistance to DNA-targeting, microtubule-targeting and nuclear receptor-targeting drugs, as well as to targeted therapy, HDACi, and checkpoint inhibitors. MYB proteins were associated with suppressed cell death and promotion of cell proliferation and survival. Resistance to DNA-targeting drugs includes platinum complexes, topoisomerase inhibitors, antimetabolites, PARP inhibitors, alkylating and photodynamic drugs. Microtubule-targeting drugs include vinca alkaloids and taxanes. Resistance to nuclear receptors refers to activators of GR and RAR, as well as inhibitors of AR and ER. Resistance to targeted therapy includes inhibitors of RTKs with implications for oncogenic Ras-MAPK and PI3K-AKT signaling, inhibitors of JAK-STAT signaling, as well as inhibitors of BCR/ABL tyrosine kinase and CHK. Resistance to epigenetic drugs and checkpoint inhibitors includes HDACi and anti-PD-1 antibodies. NFIB: Nuclear factor IB; HDACi: histone deacetylase inhibitors; PARP: phthalazinone-based poly (ADP-ribose) polymerase; GR: glucocorticoid receptor; RAR: retinoic acid receptor; AR: androgen receptors; ER: estrogen receptors; RTKs: receptor tyrosine kinases; MAPK: mitogen-activated protein kinase; PI3K: phosphoinositide 3 kinase; AKT: protein kinase B; JAK: Janus kinase; STAT: signal transduction activator of transcription; BCR: breakpoint cluster region protein; CHK: checkpoint kinase; PD-1: programmed death 1.