It is posited that the initiating event of amphibian regeneration of a limb, is retrodifferentiation* of what are to become the developing cells of the blastema. These cells reiterate a larval or premetamorphic ontogenic repertoire, induced by elevated levels of prolactin with adequate innervation. Subsequent redifferentiation of the blastema cells occurs, controlled by thyroxine and innervation.This temporal displacement of cellular morphologic characters in regeneration should be looked upon as a function of the ability to reiterate larval characters and subsequently metamorphose. (...) If correct, this would explain why amphibians which metamorphose only once, lose the ability to postmetamorphically regenerate. An exception to this,Xenopus laevis, an anuran which can epimorphically regenerate, to some extent, will be discussed.[/p]. (shrink)

Regeneration in arthropods and amphibians follows an analogous principle making comparisons between the two phyla possible.Larval arthropods and amphibians possess powers of epimorphic regeneration which wane for many species of these phyla with the completion of metamorphosis or the cessation of moulting. In those species which retain, post-maturationally, the ability to form a regenerative blastema, larval characteristics are carried into the adult and reproductive stages of these organisms. These include many species of: urodeles, ametabolous insects, crustaceans, myriapods and arachnids. The (...) long-standing distinction between embryonic regulation and true epimorphosis would thus appear to be a difference of degree rather than kind. (shrink)

Variation or rearrangement of regulatory genes is responsible for cellular malignant change. These types of chromosomal variations also produce heterochrony or paedomorphic evolution at the organismal level. Analogously, neoplasia represents a cellular macroevolutionary event, and a tumour can be said to be an evolved population of cells. To understand this cellular evolution to malignancy, it may be necessary to go beyond a clonal selection (adaptationist) explanation of neoplastic alteration. In the pericellular environment natural selection consists of the organizational restraints of (...) surrounding cells as well as the host's immunological surveillance and non-specific monocyte-macrophage systems. Indirect evidence suggests that success for the neoplasm depends not upon clonal selection, but solely upon a genetic methodology—the function of which is to elude selection.The author has coined the term cellular heterochrony to illustrate analogic similarities in the molecular modes of speciation between anaplastic cancer cells and the heterochronic evolution of organisms. By reverting to a juvenile (embryonic) repertoire of cellular behaviour a tumour secures its own tenure or niche by usurping the host's armamentarium of selection forces, employing many of the same or similar methods by which implanting and invading tissues of the mammalian embryo forestall maternal detection and rejection. A number of ways by which the tumour blocks, subverts or evades selection are discussed. (shrink)