Abstract
PurposeNative stem cells can be periodically replaced during short and long epigenetic intervals. Cancer-prone new stem cells might bring about periodic (non-stochastic) carcinogenic events rather than stochastic events. We investigated the epigenetic non-stochastic carcinogenesis by analyzing regular fluctuations in lifelong cancer incidence.Materials and MethodsKorean National Cancer Screening Program data were collected between 2009 and 2016. Non-linear and log-linear regression models were applied to comparatively evaluate non-stochastic and stochastic increases in cancer incidence. Prediction performances of regression models were measured by calculating the coefficient of determination, R2.ResultsThe incidence of gastric and colorectal cancers fluctuated regularly during both short (8 years) and long (20 years) intervals in the non-linear regression model and increased stochastically in the log-linear regression model. In comparison between the 20-year interval fluctuation model and the stochastic model, R2 values were higher in the 20-year interval fluctuation model of men with gastric cancer (0.975 vs. 0.956), and in the stochastic model of men with colorectal cancer (0.862 vs. 0.877) and women with gastric cancer (0.837 vs. 0.890) and colorectal cancer (0.773 vs. 0.809). Men with gastric cancer showed a high R2 value (0.973) in the 8-year interval fluctuation model as well.ConclusionLifelong incidence of gastrointestinal cancer tended to fluctuate during short and long intervals, especially in men with gastric cancer, suggesting the influence of an epigenetic schedule.
Highlights
Cancer is thought to arise via a multistage process involving the sequential accumulation of random carcinogenic events [1, 2]
A total of 44,998,900 men and 46,838,806 women aged ≥40 years were invited to participate in the Korean National Cancer Screening Program (KNCSP) for gastric cancer between 2009 and 2016 (Table S1)
The male-to-female ratio of cancer incidence rates increased steadily to peak at similar ages for gastric cancer (62–63 years) and colorectal cancer (64–65 years) (Figure 1C)
Summary
Cancer is thought to arise via a multistage process involving the sequential accumulation of random carcinogenic events [1, 2]. Age-specific cancer incidence increases exponentially after 40 years [3]. A stochastic multistage model has proposed that a set of random carcinogenic events triggers an exponential increase in the incidence of cancer [4]. It is noteworthy that earlyonset gastrointestinal cancers commonly arise without precancerous lesions [7, 8]. Of the two Periodic Cancerization in Gastrointestinal Cancer distinct types of gastric cancer, diffuse and intestinal, diffuse-type cancer is associated with an early onset of cancer without accompanying precancerous lesions [9]. Lifelong carcinogenesis begins to accelerate after the age of 40, and de novo carcinogenesis is prominent during the early period of accelerated carcinogenesis
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