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. 2022 Mar 4;15(2):183–193. doi: 10.21053/ceo.2021.02215

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Copyright © 2022 by Korean Society of Otorhinolaryngology-Head and Neck Surgery

This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 3. — Different regulation patterns of the PI3K and mitogen-activated protein kinase (MAPK) signaling pathways according to the partner genes of RET fusion. (A) Bar plot showing the fusion count across papillary thyroid cancer (PTC) tumors. (B) Outlier analysis of RET fusion. Blue and red dots indicate the expression of the RET gene in samples without and with fusions, respectively. (C) Impacts of the two partner genes of RET fusion on the MAPK and PI3K pathways. “Common” indicates overlapping genes in both pathways. Circles and squares indicate cis- and trans-acting genes, but there is no cis-interaction, and their sizes indicate the significance of the P-value. (D, E) The genes regulated by RET fusion of CCDC6 and NCOA4 may bridge the MAPK signaling pathway. (D) PTC in the Korean Thyroid Cancer (KTC) cohort. (E) The Thyroid Carcinoma cohort from the Cancer Genome Atlas (TCGA-THCA). (F) Two ways that RET fusion regulates MAPK signaling with different partner genes. WT, wildtype.