fig2

Figure 2. RET and RET-related cancers (adapted from Morandi et al.^[60], 2011). On the left: physiological activation of RET receptor tyrosine kinase with the representation of the molecules interacting in the formation of the complex that activates the intracellular cascade. All the RET domains, namely cadherin-like, cystein-rich, transmembrane and tyrosine kinases domains, are represented together with the calcium binding site. On the right: RET involvement in cancers. Germline and somatic point mutations cause MEN2 and MTC, respectively; the overexpression of the receptor has been observed in breast cancer, both ERα and endocrine resistant, and in prostate and pancreatic cancers; the fusion between the intracellular part of RET and the amino-terminal of different proteins cause PTC and NSCLC