Fig. 1: RET inhibition in RET-mutant solid cancers.
From: The evolution of RET inhibitor resistance in RET-driven lung and thyroid cancers
a The distribution of RET fusions and mutations (somatic or germline) in the study cohort by affected cancer type. PD, poorly differentiated; LCNEC, large cell neuroendocrine carcinoma of the lung; non-LCH, non-Langerhans cell histiocytosis of the skin; HGNEC, high-grade neuroendocrine carcinoma of the rectum. b The structure of all unique RET fusions in the study cohort (at right, number of affected cases). In light gray is the sequence from the indicated fusion partner. Red line demarcates fusion breakpoint. c Somatic mutations and germline variants (top and bottom, respectively) in two key regions of RET (left and right, respectively) in 31,447 prospectively sequenced human cancers. Labeled mutations correspond to enrolled patients. The mutational origin is indicated by the legend. Protein domains colored and indicated as in panel (b). d The clinical response of patients with RET-fusion or -mutant tumors to selpercatinib therapy is shown.
