Fig. 1: Epigenetic age acceleration (EAA) in survivors of childhood cancer treated with (n = 750) and without (n = 633) central nervous system directed therapy compared with non-cancer controls (n = 282). | Nature Communications

Fig. 1: Epigenetic age acceleration (EAA) in survivors of childhood cancer treated with (n = 750) and without (n = 633) central nervous system directed therapy compared with non-cancer controls (n = 282).

From: Epigenetic age acceleration, telomere length, and neurocognitive function in long-term survivors of childhood cancer

Fig. 1: Epigenetic age acceleration (EAA) in survivors of childhood cancer treated with (n = 750) and without (n = 633) central nervous system directed therapy compared with non-cancer controls (n = 282).

Marginal adjusted means and 95%CI (error bars) from linear regression models (t-test, two-sided, no adjustment for multiple comparisons) adjusted for sex, body mass index, smoking, and physical activity. Regardless of exposure to CNS-directed therapy, survivors experienced significantly higher EAA, faster DundedinPACE, and shorter mean leukocyte telomere length compared with non-cancer controls (all p < 0.001), full results can be found in Supplementary Table 2. Source data are provided as a Source data file.

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