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. Author manuscript; available in PMC: 2015 Jan 23.
Published in final edited form as: Leuk Lymphoma. 2011 Mar 7;52(7):1321–1335. doi: 10.3109/10428194.2011.559802

Figure 3.

Figure 3

Comparison of recurrent genomic copy number imbalances in canine and human BCL. a) summarizes the genome-wide incidence of copy number gain and loss in the 80 cDLBCL cases from the present study, according to their dog chromosomal location. Gains of CFA 13 and CFA 31 are highlighted in blue and pink, respectively. In b) the same canine data are replotted according to the equivalent location of arrayed loci on the corresponding human chromosome. When recoded into orthologous human genome co-ordinates, gain of CFA 13 now manifests as partial gains on HSA 4 and 8 (highlighted in blue) and gain of CFA 31 manifests as gain of HSA 21 (highlighted in pink). Figure c) shows data in a comparable format derived from a prior study of 46 hDLBCL cases [22]. In d) and e) these 46 hDLBCL cases are segregated to compare the cytogenetic profiles of the 28 hABC-DLBCL cases and the 18 hGCB-DLBCL cases, respectively. These images demonstrate the apparently reduced degree of genomic imbalance detected in cBCL compared to its human counterpart, and reveals evidence for shared aberrations (including gain of MYC) as well as aberrations that are not shared (such as deletion of CDKN2A/B).