title: Just like the rest of evolution in Mother Nature, the evolution of cancers may be driven by natural selection, and not by haphazard mutations.
abstract: Sporadic carcinogenesis starts from immortalization of a differentiated somatic cell or an organ-specific stem cell. The immortalized cell incepts a new or quasinew organism that lives like a parasite in the patient and usually proceeds to progressive simplification, constantly engendering intermediate organisms that are simpler than normal cells. Like organismal evolution in Mother Nature, this cellular simplification is a process of Darwinian selection of those mutations with growth- or survival-advantages, from numerous ones that occur randomly and stochastically. Therefore, functional gain of growth- or survival-sustaining oncogenes and functional loss of differentiation-sustaining tumor suppressor genes, which are hallmarks of cancer cells and contribute to phenotypes of greater malignancy, are not drivers of carcinogenesis but are results from natural selection of advantageous mutations. Besides this mutation-load dependent survival mechanism that is evolutionarily low and of an asexual nature, cancer cells may also use cell fusion for survival, which is an evolutionarily-higher mechanism and is of a sexual nature. Assigning oncogenes or tumor suppressor genes or their mutants as drivers to induce cancer in animals may somewhat coerce them to create man-made oncogenic pathways that may not really be a course of sporadic cancer formations in the human.
authors.affiliation: CAS Key Laboratory of Genome Sciences and Information, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, P.R. China.
authors.forename: Ju
authors.initials: J
authors.lastname: Zhang
authors.affiliation: CAS Key Laboratory of Genome Sciences and Information, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, P.R. China.
authors.forename: Xiaomin
authors.initials: X
authors.lastname: Lou
authors.affiliation: Hormel Institute, University of Minnesota, Austin, MN 55912, USA.
authors.forename: Lucas
authors.initials: L
authors.lastname: Zellmer
authors.affiliation: CAS Key Laboratory of Genome Sciences and Information, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, P.R. China.
authors.forename: Siqi
authors.initials: S
authors.lastname: Liu
authors.affiliation: Laboratory of Cell and Molecular Biology, Cancer Institute, Chinese Academy of Medical Science, Beijing 100021, P.R. China.
authors.forename: Ningzhi
authors.initials: N
authors.lastname: Xu
authors.affiliation: Hormel Institute, University of Minnesota, Austin, MN 55912, USA.
authors.forename: D Joshua
authors.initials: DJ
authors.lastname: Liao
keywords: cancer; evolution; mutation; oncogenes; tumor suppressor genes