Should we consider cancers as embryonic diseases or as consequences of stem-cell deregulation?

Abstract

Cancers have long been described as the result of successive selections of somatic cells progressively acquiring growth and survival advantages. Such a model was hardly compatible with the obvious heterogeneity of the cancer cell population present in tumors. This heterogeneity rather suggests that mutations hint multipotent cells that, in addition to the resulting proliferation and survival advantages, display differentiation capabilities. Adult stem cells or progenitors display similar properties, supporting the concept that cancers actually originate from these cells. The recent observation that differentiated cells can dedifferentiate and acquire stemness properties suggests an alternative and additional explanation for the origin of “cancer-initiating” cells and reopens the debate of the contribution of somatic cells to cancer progression.