Figure 9.

Age acceleration in colorectal cancer, glioblastoma multiforme and acute myeloid leukemia. (A-F) Results for colorectal cancer. Mean age acceleration (y-axis) in colorectal cancer versus mutation status (denoted by a plus sign) in (A)BRAF, (B)TP53, (C)K-RAS. (D) Promoter hyper methylation of the mismatch repair gene MLH1 (denoted by a plus sign) is significantly (P = 5.7E-5) associated with age acceleration. (E) Mean age acceleration across different patient groups defined by combinations of BRAF, TP53, K-RAS, MLH1 status. The first bar reports the age acceleration in normal adjacent colorectal tissue from cancer patients but the sample size of 4 is rather low. (F) CpG island methylator phenotype is associated with age acceleration (P = 3.5E-5). (G-R) Results for various genomic abnormalities in glioblastoma multiforme. (J) A highly significant (P = 3.3E-7) relationship can be found between H3F3A mutations and age acceleration. Samples with a G34R mutation have the highest age acceleration. (S-W) Results for various genomic aberrations in acute myeloid leukemia. (X) Thyroid cancer age acceleration versus RAS family mutation status is inconclusive since mutation status was largely unknown. Error bars represent 1 standard error.

Horvath Genome Biology 2013 14:R115   doi:10.1186/gb-2013-14-10-r115
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