Cancer clonality and field theory.
We discuss a "genomic" mechanism capable of yielding clonal malignancies (e.g. hemopoietic leukemias) without the prerequisite of multiple or single mutations. This hypothetical mechanism is based upon the anachronistic (illegal) expression of a special gene P, where P stands for "potential". P. is a stimulus promoting renewal of stem and most immature cells of hemopoietic tissues. In normal conditions, these cells renew themselves only after receiving P from special microenvironmental cells or field "sources". When illegally expressed by a previously dependent cell, the autocatalyzed potential competes with differentiating factors and slows down terminal differentiation. This sets the cell on a temporary (or extended) "limit cycle" between competing attractors viz: renewal and extinction, whereby both progenitor and clonal progeny are locked between continuous proliferation and terminal differentiation for a time longer than their normal, absolutely source dependent counterparts.
Matioli
G T
GT
USC Medical School, Los Angeles 90033.
D002454:Cell Differentiation; D002471:Cell Transformation, Neoplastic; D002999:Clone Cells; D005786:Gene Expression Regulation; D006412:Hematopoietic Stem Cells; D006801:Humans; D007938:Leukemia / Q000235:genetics*; D008957:Models, Genetic