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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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Extended Data Fig. 4 — a, Sashimi plot showing FGFR2 read coverage and junction reads of the FMI sample #1 (COAD). FGFR2-I17 RE to intergenic space was diagnosed by FMI, and discordant FGFR2-TACC2 in-frame fusion with FGFR2-E17 to TACC2-E19 junction was found with hybrid-capture RNA-seq. Green arrows indicate FGFR2 BP identified with panel-seq. b, Sashimi plot showing FGFR2 read coverage and junction reads of the FMI sample #2 (STAD). FGFR2-E1–E17 partial amp was diagnosed by FMI, and high FGFR2 expression with few E17–E18 junction reads but E18-C3 usage was found with hybrid-capture RNA-seq. Purple arrows indicate partially amplified FGFR2 region identified with panel-seq. c, FGFR2 amp status and RE type distribution in samples with FGFR2 REs (n = 50) found in the pan-cancer cohort from The Cancer Genome Atlas (TCGA, n = 10,344 samples). Dotted red line, RE read frequency threshold (> 0.15) to call samples expressing FGFR2^ΔE18 REs (n = 17). d, 67 samples (0.65% incidence) containing FGFR2^ΔE18 in-frame fusions (n = 12, 0.12% incidence), FGFR2^ΔE18 non-canonical REs (n = 5, 0.05% incidence), proximal FGFR2-E18-truncating mutations (n = 1, 0.01% incidence), and cases with significant FGFR2-E18-C3 (n = 40; E18-C3 usage only, n = 36, 90% of total, 0.35% incidence; E18-C3 usage + RE, n = 4, 10% of total, 0.05% incidence) and/or E18-C4 (n = 13, 0.13% incidence) usage found in TCGA cohort. Asterisks mark previously annotated FGFR2 in-frame fusions⁹¹. exp, expression; GBM, glioblastoma multiforme; KIRC, kidney renal clear cell carcinoma; KIRP, kidney renal papillary cell carcinoma; LIHC, liver hepatocellular carcinoma; SKCM, skin cutaneous melanoma; THYM, thymoma. e, Frequencies (top panel) and distributions (bottom panel) per tumour type of expressed FGFR2^ΔE18 alterations found in TCGA cohort. f, g, Sashimi plots showing FGFR2 read coverage and junction reads of TCGA-BRCA samples A8-A08A (f) and BH-A203 (g) with identified FGFR2-I17 REs to intergenic space and FGFR2-E18-C3 usage.

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