{'fraction_non_alphanumeric': 0.0243161094224924, 'fraction_numerical': 0.0, 'mean_word_length': 5.241706161137441, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Contribution of epigenetic mechanisms to variation in cancer risk among tissues

Significance It is well-known that the risk of cancer varies widely between different tissues of the body with some cell types (e.g., colon, breast) being prone to cancer, whereas others (e.g., brain, bone) only rarely develop tumors, but the mechanism of this phenomenon has not been elucidated. Recently, it was shown that this risk coefficient may actually be related to the inherent number of stem-cell divisions that go into generating each individual cell type during development. In this work, we demonstrate that cancer risk is highly correlated with the degree of aberrant age-dependent methylation in normal tissues, clearly supporting the idea that cell-type tumor susceptibility may be influenced by biologically intrinsic epigenetic factors. Recently, it was suggested that tissue variation in cancer risk originates from differences in the number of stem-cell divisions underlying each tissue, leading to different mutation loads. We show that this variation is also correlated with the degree of aberrant CpG island DNA methylation in normal cells. Methylation accumulates during aging in a subset of molecules, suggesting that the epigenetic landscape within a founder-cell population may contribute to tumor formation.