Extended Data Figure 9: Expression of wild-type ALK, ALKF1174L, and EML4–ALK confers sensitivity to the ALK inhibitor crizotinib in vivo.
From: Alternative transcription initiation leads to expression of a novel ALK isoform in cancer
a–c, Bioluminescence of luciferase-labelled NIH-3T3 grafted tumours expressing wild-type ALK (a), ALKF1174L (b), or EML4–ALK (c) in SCID mice treated with either vehicle or crizotinib. Error bars, mean ± s.e.m.; n = 8 tumours; see also Source Data associated with this figure. d–f, H&E staining and immunohistochemistry of explanted tumours expressing wild-type ALK (d), ALKF1174L (e), or EML4–ALK (f) 48 h after the first crizotinib treatment. Scale bar, 50 μm. g, MSK-IMPACT assay reveals copy number alterations and loss of CDKN2A and PTEN in melanoma metastasis MM-382, but no mutations. The log2 ratio was calculated across all targeted regions by comparing the coverage in tumour versus normal. h, FISH for ALK shows no rearrangement; the 3 juxtaposed green/orange signals indicate a trisomy 2. Scale bar, 1 μm. i, The four FISH signals for MET and centromere 7 indicate a tetrasomy 7, but no MET amplification. Scale bar, 1 μm.
