Abstract

In the last decade, more and more researchers believe that cancer is caused by a progressive weakening of a multicellular cell, leading to a loss of function and a switch to a unicellular life cycle. Lineweaver et al. [1] consider cancer as “a dysregulation and degeneration of recently evolved genes and the upregulation of complementary ancient genes.” This also applies to DNA repair genes. Multicellular cells have differentially dysfunctional DNA repair systems [2]; second, more evolved repair genes (evolutionary younger genes) become dysfunctional more rapidly than older genes. Also of particular interest is the consideration by Lineweaver et al. [1] that cancer “can only revert to phenotypes compatible with cellular survival in a human” [3]. This fits with the analogy described between the dual cell systems of cancer and intestinal parasitic amoebae [4-9].

Keywords: Cancer; Germline; Cancer germ stem cells; Genome repair; PGCC; EMT; MET

Abbreviations: aCLS: Autonomous Cyst-Like Structure; CAM: Cell Agglutinating Molecules; DSB: Double Strand Break; GSC: Germ Stem Cells; MGRS: Multinucleated Genome Repair Structure; PGCC: Polyploid Giant Cancer Cell; SGT: Soma-To-Germ Transition