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Monoclonal tumor origin is an underlying misconception of the RESIC approach

Attolini et al. (1) recently reported a computational approach named retracing the evolutionary steps in cancer (RESIC), the purpose of which is to “deduce the temporal sequence of genetic events during tumorigenesis from cross-sectional data of tumors at their fully transformed stage” (1). The authors (1) indicated that they chose colon cancer as a model in which to validate their approach because there is an “established sequence of genetic events during the multistep process of colon carcinogenesis” (1). The basic premise underlying the RESIC approach (that initial events can be ordered based on the frequency of events in fully transformed tumors) is flawed. In developing the RESIC approach, the authors (1) have not considered a critical aspect of carcinogenesis, specifically, that many, or perhaps most, tumors are polyclonal in origin (2). Ironically, definitive evidence that tumors are polyclonal comes from the colon cancer model (2–4). Despite convincing evidence from human studies (3), consistent findings in rodent models (4), and multiple reviews on polyclonal tumor origin (ref. 2 has additional citations), monoclonal tumor origin too often remains an unacknowledged underlying premise in the field of oncology.