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. 2019 Dec 2;18:1176935119890290. doi: 10.1177/1176935119890290

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© The Author(s) 2019

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 2. — (A) A whole genome interaction view of neuroblastoma copy number (CN) associations (chr1-X). Boxed regions highlight chr2 (enlarged in Figure 3), chr11, and the negatively signed off-diagonal association of 11q and 17q. (B) The enlarged chr11-chr17 map illustrates the strong anticorrelated regions of 11q-17q. The lowest correlation point is highlighted (r =−0.482, Benjamini-Hochberg adjusted P value is .000117). The number of tests used for the adjustment is the number of bin pairs in the whole genome. (C) Representative regression plot of CN values on 11q and 17q illustrates an anticorrelation trend as well as the detailed sample-level data on 3 tooltips. (D) The data from the same coordinates as (C) are represented as a histogram showing clear separation of CN value distributions on 11q and 17q. These plots support the interpretation that there is a significant association of 11q loss with 17q gain.