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. 2022 Aug 10;608(7923):609–617. doi: 10.1038/s41586-022-05066-5

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© The Authors 2022, corrected publication 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — a, Analysis of 3,067 samples (1.23% incidence) containing FGFR2-I17/E18 in-frame fusions (n = 757, 0.30% incidence), frame unknown REs (n = 82, 0.03% incidence), intergenic space REs (n = 291, 0.12% incidence), out-of-strand REs (n = 88, 0.04% incidence), internal REs (n = 29, 0.01% incidence), FGFR2-E18 splice-site mutations (mut; n = 21, 0.01% incidence), E18-truncating nonsense and frameshift mutations (proximal, n = 59, 0.02% incidence; distal, n = 23, 0.01% incidence), FGFR2-E1–E17 partial amplifications (amp; n = 73, 0.03% incidence), E1–E18 full-length amplifications (n = 838, 0.34% incidence), and/or FGFR2 missense hotspot mutations affecting Ser252, Cys382, Asn549 or Lys659 (n = 978, 0.39% incidence) found in 249,570 pan-cancer diagnostic panel-seq profiles from FMI. BLCA, bladder urothelial carcinoma; BRCA, breast invasive carcinoma; CESC, cervical squamous cell carcinoma and endocervical adenocarcinoma; CHOL, cholangiocarcinoma; chr, chromosome; COAD, colon adenocarcinoma; ESCA, oesophageal carcinoma; HNSC, head and neck squamous cell carcinoma; LUAD, lung adenocarcinoma; LUSC, lung squamous cell carcinoma; OV, ovarian serous cystadenocarcinoma; PAAD, pancreatic adenocarcinoma; PRAD, prostate adenocarcinoma; READ, rectum adenocarcinoma; SARC, sarcoma; SGC, salivary gland carcinoma; STAD, stomach adenocarcinoma; UCEC, uterine corpus endometrial carcinoma; UCS, uterus carcinosarcoma. b, Global phosphoproteomic analysis of NMuMG cells expressing GFP or the indicated Fgfr2 variants. Groups were compared in a pairwise manner using the robust kinase activity inference (RoKAI) tool, including two-tailed hypothesis testing on Z-scores and false-discovery rate (FDR) multiple-testing correction using the Benjamini–Hochberg method. Group-comparison fold change (FC) values of −1.5 ≥ FC ≥ 1.5 and P < 0.05 were considered. The heatmaps show phosphosites subselected from the RoKAI output and grouped into the indicated signalling pathways guided by RoKAI as colour-coded row Z-scores calculated from log₂-transformed intensity values. c–e, Kaplan–Meier curves showing mammary-tumour-free survival of female mice intraductally injected with lentiviruses encoding the indicated Fgfr2 variants. Cohort counts (n) are injected mammary glands (MGs) per number of mice. The Fgfr2^FL and Fgfr2^ΔE18 curves in c are duplicated in d and e. P values were calculated using log-rank (Mantel–Cox) tests; ****P < 0.0001; NS, not significant (P ≥ 0.05).

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