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. Author manuscript; available in PMC: 2021 Dec 1.
Published in final edited form as: Trends Cancer. 2021 Aug 12;7(12):1074–1088. doi: 10.1016/j.trecan.2021.07.003

Figure 1. Rearranged during transfection (RET) pathway and acquired resistance mechanisms (red arrow) to selective RET inhibitors in RET-aberrant cancers.

Figure 1.

Abbreviations: AKT, protein kinase B; ART, artemin; c-Met, mesenchymal epithelial transition factor; c-Myc, avian myelocytomatosis virus oncogene cellular homolog; CLD 1–4, cadherin-like domain 1–4; CRD, cysteine-rich domain; EGFR, epidermal growth factor receptor; ERK, extracellular signal-regulated kinases; GDNF, glial derived neurotrophic factor family ligands; GFRα 1–4, GDNF family alpha receptors 1–4; JAK, Janus kinase; KRAS, Kirsten rat sarcoma 2 viral oncogene homolog; MAPK pathway (RAF/MEK/ERK), mitogen-activated protein kinase pathway; MEK, MAPK/ERK kinase; mTOR, mammalian target of rapamycin; NTN, neuturin; NTRK, neurotrophic tyrosine receptor kinase; PI3K, phosphatidylinositol 3-kinase; PSP, persephin; RAF, rapidly accelerated fibrosarcoma; RTK, receptor tyrosine kinase; STAT, signal transducer and activator of transcription; TK, tyrosine kinase; TM, transmembrane.