The strength of organ, tissue, and body field effects determines the frequency of all neoplasia

Abstract

In 1953, Danely Slaughter proposed the concept of field cancerization, or field effect, to explain the development of additional neoplasia of similar type. A recent theory (de Groen, 2022) states that all DNA is exposed to a constant source of damage, resulting in a constant rate of germline and somatic DNA mutations. If the field effect and constant mutation theories are correct and a single somatic mutation causes the transition from non-neoplastic to neoplastic phenotype, then all rates of neoplasia formation can be modeled by exponential equations containing a single variable that determines the chance of phenotype transition. In this perspective, studies from 1953 till 2021 originating from America, Europe, and Asia about head, chest, abdomen, pelvic, and skin neoplasia were reviewed and showed consistent field effects that are modeled by tapering exponential equations containing a single variable defining field effect strength; Pearson and linear correlation coefficients for observed and modeled data range from 0.994 to 1. Thus, existing data are compatible with a constant rate of DNA damage. Organ-specific, tissue-specific, or body-wide mutagenesis conditions determine the rate of neoplasia development and explain the co-occurrence of seemingly unrelated neoplasia at predictable frequencies. Shared risk factors explain increased risk for additional neoplasia in persons with one neoplastic lesion.