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<p>The rising global incidence of early-onset cancers (EOCs)—defined as malignancies diagnosed before age 50—represents an urgent and complex public health challenge. Once considered rare, EOCs are increasing across diverse tumor types, particularly colorectal, breast, gastric, thyroid, and pancreatic cancers, in both high-income and low- and middle-income countries. While improved detection may explain part of this trend, emerging evidence suggests deeper etiological roots linked to early-life exposures, epigenetic reprogramming, immune modulation, and gut microbiome alterations. Modern environmental and lifestyle shifts—including diet, sedentary behavior, circadian disruption, and antibiotic use—may initiate tumorigenic pathways decades before diagnosis. Polygenic risk scores further point to gene–environment interactions, reinforcing the need for syndemic models that integrate social, biological, and ecological dimensions. However, major research gaps persist. Many pediatric cohorts lack long-term follow-up, and early-life biospecimens remain underutilized. Artificial intelligence offers promise for integrating complex life-course data to inform precision prevention. Clinically, EOCs often present with more aggressive phenotypes, raising questions about age-appropriate screening and care models. Broader responses must address structural drivers of risk, from food systems to labor conditions. Multisectoral action is needed to protect future generations. Understanding EOCs as the early signal of a broader chronic disease wave demands a proactive, life-course–oriented public health response.</p>

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Early onset cancer and its growing impact on public health across generations

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月5日

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  • Luís Carlos Lopes-Júnior,
  • Wesley Rocha Grippa,
  • Vitor Fiorin Vasconcellos

摘要

The rising global incidence of early-onset cancers (EOCs)—defined as malignancies diagnosed before age 50—represents an urgent and complex public health challenge. Once considered rare, EOCs are increasing across diverse tumor types, particularly colorectal, breast, gastric, thyroid, and pancreatic cancers, in both high-income and low- and middle-income countries. While improved detection may explain part of this trend, emerging evidence suggests deeper etiological roots linked to early-life exposures, epigenetic reprogramming, immune modulation, and gut microbiome alterations. Modern environmental and lifestyle shifts—including diet, sedentary behavior, circadian disruption, and antibiotic use—may initiate tumorigenic pathways decades before diagnosis. Polygenic risk scores further point to gene–environment interactions, reinforcing the need for syndemic models that integrate social, biological, and ecological dimensions. However, major research gaps persist. Many pediatric cohorts lack long-term follow-up, and early-life biospecimens remain underutilized. Artificial intelligence offers promise for integrating complex life-course data to inform precision prevention. Clinically, EOCs often present with more aggressive phenotypes, raising questions about age-appropriate screening and care models. Broader responses must address structural drivers of risk, from food systems to labor conditions. Multisectoral action is needed to protect future generations. Understanding EOCs as the early signal of a broader chronic disease wave demands a proactive, life-course–oriented public health response.