Evading growth suppression |
Cyclin-dependent kinase inhibitors: CDK4/6 inhibitors |
Sustained proliferative signaling |
Blocking growth factor receptor pathways (i.e., EGFR and others): monoclonal antibodies, tyrosine kinase inhibitors |
Resisting cell death |
BH3-mimetics that specifically bind to the hydrophobic groove of BCL-2: venetoclax |
Enabling replicative immortality |
Inhibition of telomerase activity, induction of senescence in tumor cells: a number of commonly used cancer therapeutics are involved in induction of senescence in cancer cells |
Deregulating cellular energetics |
Inhibition of aerobic glycolysis, inhibition of isocitrate dehydrogenase (IDH) and others: IDH1 and IDH2 inhibitors |
Genome instability and mutation |
PARP inhibition to facilitate synthetical lethality in homologous recombination deficient tumor cells: PARP inhibitors |
Inducing angiogenesis |
Inhibition of angiogenic pathways (i.e., VEGF, PlGF): monoclonal antibodies, fusion constructs, tyrosine kinase inhibitors |
Activating invasion and metastasis |
Targeting the epithelial- mesenchymal transition (EMT) program (e.g., HGF/cMET inhibition), anti-angiogenic treatment strategies |
Avoiding immune destruction |
Immune activation: immune checkpoint antibodies (i.e., anti-PD-1, anti-PD-L1, anti CLTA-4) |
Tumor promoting inflammation |
Selective anti-inflammatory drugs: not yet available clinically |