Is a bi-clonal interaction, analogous to that underlying embryogenesis the origin of the earliest malignant phenotype?
We propose a theoretical model of carcinogenesis which parallels embryonic induction. It is based on the interaction between two clones of cells. One of them is of germ cell ancestry and is the source of transforming effector cells. The second clone is the potential target of such travelling "lymphocytoid" cells and emerges in tissues exhibiting the precancerous picture of dysplasia. In atypical fields each endopolyploid cell, arrested in G2 and involved in genomic changes, is the stem of a clonal growth. This emerging new phenotype is subjected to policing control by wandering effector cells. This situation establishes the probability of a random collision between two cells pertaining to different lineages, with two possible antithetical results, cytolysis or cell fusion comparable to fertilization. The latter event is suggested to determine malignancy.
D000818:Animals; D002470:Cell Survival; D002471:Cell Transformation, Neoplastic; D002999:Clone Cells / Q000166:cytology; D054278:Embryonal Carcinoma Stem Cells; D004627:Embryonic Induction; D005260:Female; D005306:Fertilization; D005854:Germ Cells / Q000166:cytology; D006801:Humans; D008297:Male; D008954:Models, Biological; D009369:Neoplasms / Q000209:etiology*; D014411:Neoplastic Stem Cells / Q000166:cytology; D010641:Phenotype