Integrating the ideas of life course across cellular, individual, and population levels in cancer causation.
Cells, individuals, and societies are complex systems in which the integrity of structure and function is protected through tight regulation and control. For each level of organization, health represents the ability to maintain integrity in response to the wider environment. Critical stages during growth and development act as checkpoints, where choice is exercised, and help determine future direction. Important among factors influencing the checkpoints include the availability of nutrients or foods within the immediate environment. At the cellular and whole-body levels, this information can be communicated to future generations. Recent work on the developmental origins of adult disease indicate specific factors that set limits on structure and function and potentially limit the capacity of the cell and individual to respond to environmental stressors that represent potential risk factors for neoplastic change. Epigenetic mechanisms modulate structure and function at the cellular and tissue levels, reflecting the potential for the growth and development of individuals, and reflect the food and nutrients available to the body as a whole and within the wider society. Understanding the nature and the interaction of the critical factors that determine and regulate variable stable and unstable gene expression will be increasingly important in characterizing abnormal cellular function and risk of disease for individuals and populations. This will require the ability to synthesize large data sets within and between different levels of organization to develop and refine a deeper understanding of how the systems are effectively integrated and regulated within and across generations and where this fails in the genesis of cancer.
Jackson
Alan A
AA
Institute of Human Nutrition, University of Southampton, Southampton, UK. aaj@soton.ac.uk
D000818:Animals; D001823:Body Composition; D004777:Environment; D044127:Epigenesis, Genetic / Q000502:physiology*; D006801:Humans; D008018:Life Cycle Stages; D008954:Models, Biological; D009369:Neoplasms / Q000209:etiology* / Q000235:genetics; D009765:Obesity / Q000150:complications; D011159:Population Surveillance