About six weeks ago, I wrote a post on An Evolving Ecosystem Model of Neoplasms… now another article looking at parallels between natural selection and cancer progression has appeared in a relatively obscure (to me) journal (Medical Hypotheses): Recursive causality in evolution: A model for epigenetic mechanisms in cancer development.
The story goes something like this: in light of recent advances in evo-devo, and molecular biology/oncology into epigenetic mechanisms of development and cancer, and that it might be useful to consider both in terms of not just a series of acquired, step-by-step, genetic mutations, but acquired epi-genetic modifications as well.
In the last decade, amazing advances have shown that both evolution and cancer progression involve changes in where and how key proteins are used in cells and systems, at least as much as changes in the proteins themselves.
Haslberger et al. focus on a Systems theory of evolution, applying a notion of “recursive” or “feedback” causality (the idea that every biological effect in living systems, in some way, feeds back to its own cause). Essentially, however, they’re talking about the black box between genotype and phenotype and its application not only to evolution, but also to disease. This goes for both the role of epigenetic changes in acquiring new phenotypes, to also generating variation for natural selection to act upon at the cellular level.
So, without ignoring genetic changes (such as the role of various point mutations or aberrant fusion proteins in cellular dysfunction), there is a need to focus on activities that up- or -down regulate important pathways in malignancy and tumor suppression. Haslberger et al. focus on DNA-methylation and histone modification, both as mechanisms of malignant development and as prognostic indicators of risk.
Damn neat how Evo-Devo and Oncology are starting to lend support to each other, isn’t it?
- Recursive causality in evolution: A model for epigenetic mechanisms in cancer development. Haslberger A, Varga F, Karlic H. Med Hypotheses. 2006 Jul 14; [Epub ahead of print]. Pubmed.
- The cell clone ecology hypothesis and the cell fusion model of cancer progression and metastasis: history and experimental support. Parris GE. Med Hypotheses. 2006; 66(1):76-83. Pubmed.