Definitions of some key words
| Key Word | Definitions |
|---|---|
| Allosteric site | A regulatory site on the protein’s surface is distinct from the substrate, ligand, or partner binding sites (Nussinov and Tsai, 2015). |
| Clinically actionable mutation | A mutation alters clinical responses (e.g., survival or drug responses) in patients harboring this mutation. |
| Driver mutation | A mutation directly or indirectly promotes a selective growth or survival to the cell in which it occurs. |
| Edgetic alleles | Genetic alterations (mutations) alter specific macromolecular interactions (“edges”) rather than affecting folding and stability of proteins (Sahni et al., 2015). Edgetic mutations include “node” removal by truncating mutations (Zhong et al., 2009) and in-frame edgetic mutations that disrupt interactions between proteins, DNA, or RNA. |
| Network-attacking mutations | Mutations alter signaling networks via different types of network perturbations: signaling network dynamics, network structure, and dysregulation of phosphorylation sites (Creixell et al., 2015). |
| Orthosteric site | The primary, unmodulated binding site (on a receptor) of a ligand, such as adenosine triphosphate (ATP) binding site of a kinase. |
| Personal mutanome | A personal mutanome is a portfolio of DNA sequencing data (e.g., whole exome or whole genome), protein structural genomics, and interpretation of mutational landscape of an individual patient. |
| Personalized medication | Interventions or/and products are tailored to the individual patients based on their predicted response or risk (e.g., particularly genomic or molecular profiles as clinically actionable biomarkers) of disease. |
| Spliceosome mutations | Hotspot somatic mutations affect genes encoding RNA splicing factors (Dvinge et al., 2016). |
| Undruggable | A protein could not be targeted pharmacologically. More appropriate terms might be “difficult to drug” or “yet to be drugged.” |