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. Author manuscript; available in PMC: 2017 Jul 15.
Published in final edited form as: Clin Cancer Res. 2016 Feb 29;22(14):3593–3605. doi: 10.1158/1078-0432.CCR-15-2296

Figure 1.

Figure 1

Schematic illustration of the structure of MYC gene and Myc protein, and the composition and occurrence of MYC mutations. (A) Three MYC exons (top) are transcribed into an mRNA (middle) with untranslated regions (UTR) and the coding sequence (CDS), and then translated into the Myc protein with MYC box I (MBI, 44–63 aa) and MYC box II (MBII, 128–143 aa) in the N-terminal domain (NTD), MYC box III (MBIII including A and B), nuclear localization sequence (NLS), and the basic helix-loop-helix leucine zipper motif (B-HLH-LZ, 355–439 aa, involved in the dimerization with MAX and interacting with other HLH proteins) motif in the C-terminal domain (CTD). TAD indicates transactivation domain. (B) Occurrence of the SNPs (indicated in parentheses) in the 5´UTR, CDS and 3´UTR found in the DLBCL cohort. The SNP nucleotide positions are according to the translation start site resulting in the canonical Myc protein (439 aa). (C) Comparison of the mutation rate of 10 genes we sequenced for the DLBCL cohort. (D) Patterns of the MYC variations (SNPs and somatic mutations) found in the DLBCL cohort. (E) Proportions of silent, missense, nonsense, frame-shift, and splicing mutations in the MYC CDS found in the DLBCL cohort. (F) Frequencies of missense and nonsense Myc mutations. Numbers in parentheses indicate occurrence in the DLBCL cohort.