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. 2018 Jan 23;2:PO.17.00143. doi: 10.1200/PO.17.00143

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© 2018 by American Society of Clinical Oncology

Licensed under the Creative Commons Attribution 4.0 License: http://creativecommons.org/licenses/by/4.0/

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Fig 1. — (A) Oncoprint of germline and somatic mutations in mismatch repair (MMR) genes and in POLE in the Lynch cohort. (B) Mutational decomposition analysis of the samples with ≥ 10 somatic mutations. (*) Hypermutated sporadic upper-tract urothelial carcinoma (UTUC) tumor with a hotspot mutation in POLE. (C) Microsatellite instability (MSI) sensor scores across the two cohorts. (D) Frequency of somatic alterations in Lynch syndrome–associated (n = 17) and sporadic UTUC (n = 82) cohorts. AID/APOBEC, activation-induced cytidine deaminase/apolipoprotein B mRNA-editing enzyme catalytic polypeptide; CNV, copy-number variation; DDR, DNA damage repair; NS, non significant; RCC, renal cell carcinoma.