Childhood, adolescent, and early adult exposures and cancer risk in middle to late adulthood.

Although most common cancers occur in adulthood, evidence supports that the etiological relevant time period for many cancers can often extend into childhood and adolescence. This fact is especially noteworthy given the recent rise in early-onset cancers, generally defined as cancers before age 50. Two factors could contribute to strong early life influences on cancer. First, an organ may have a specific susceptibility to irreversible genetic damage from exposure at an early life stage. Second, cells with genetic damage established earlier in life will have sufficient time available to transform into cancer because many cancers require multiple decades to fully develop after initiation, and cancers from cell initiated later in life may be averted by competing causes of death. This paper reviews the main types of evidence supporting that both reasons why early-life exposures are likely to be important. First, a brief summary of the multistage process of cancer is provided, followed by insights from the initiation-promotion model of cancer, and then evidence that some tissues may be especially prone to carcinogenic damage at early ages. The review then ends with some emerging data supporting that lifestyle exposures act primarily during adolescence for breast cancer (especially premenopausal/early onset breast cancer) because of greater carcinogenic susceptibility of breast tissue during this time period; in contrast, for colorectal cancer, lifestyle factors are operative throughout life, but early life is particularly important because early tissue damage allows longer time for cancers (especially early-onset colorectal cancer) to have sufficient time to develop.