Figure 2.
Mutational profile of tumors. (A) Resequenced somatic mutations observed in tumor exome sequencing dataset of 6 patients, A1 to 2, and L1 to 4 classified by type. (B) Frequency and type of probable driver mutations and recurrent mutations. Nonsilent mutations (missense-, nonsense-, and splicing-mutations, and frameshift/in frame insertions/deletions), which occurred in genes that are significantly mutated in ATL,14 were considered putative driver mutations (CCR4 to ZFP36L2). Patient A2 had an additional silent mutation in NOXA1; patient L2 also had silent mutations in TP53 and PIK3CD, and an intronic mutation in POT1. Genes that were recurrently mutated within the cohort were also plotted (MUC16 to ZFPM2).

Mutational profile of tumors. (A) Resequenced somatic mutations observed in tumor exome sequencing dataset of 6 patients, A1 to 2, and L1 to 4 classified by type. (B) Frequency and type of probable driver mutations and recurrent mutations. Nonsilent mutations (missense-, nonsense-, and splicing-mutations, and frameshift/in frame insertions/deletions), which occurred in genes that are significantly mutated in ATL,14  were considered putative driver mutations (CCR4 to ZFP36L2). Patient A2 had an additional silent mutation in NOXA1; patient L2 also had silent mutations in TP53 and PIK3CD, and an intronic mutation in POT1. Genes that were recurrently mutated within the cohort were also plotted (MUC16 to ZFPM2).

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