title: Maternal-fetal conflict, genomic imprinting and mammalian vulnerabilities to cancer.
abstract: Antagonistic coevolution between maternal and fetal genes, and between maternally and paternally derived genes may have increased mammalian vulnerability to cancer. Placental trophoblast has evolved to invade maternal tissues and evade structural and immunological constraints on its invasion. These adaptations can be co-opted by cancer in intrasomatic selection. Imprinted genes of maternal and paternal origin favour different degrees of proliferation of particular cell types in which they reside. As a result, the set of genes favouring greater proliferation will be selected to evade controls on cell-cycle progression imposed by the set of genes favouring lesser proliferation. The dynamics of stem cell populations will be a particular focus of this intragenomic conflict. Gene networks that are battlegrounds of intragenomic conflict are expected to be less robust than networks that evolve in the absence of conflict. By these processes, maternal-fetal and intragenomic conflicts may undermine evolved defences against cancer.
authors.affiliation: Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, MA 02138, USA dhaig@oeb.harvard.edu.
authors.forename: David
authors.initials: D
authors.lastname: Haig
mesh_terms: D000818:Animals; D005075:Biological Evolution; D005260:Female; D053263:Gene Regulatory Networks; D018392:Genomic Imprinting; D006801:Humans; D008431:Maternal-Fetal Exchange / Q000235:genetics*; D009369:Neoplasms / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D011247:Pregnancy; D012641:Selection, Genetic; D014327:Trophoblasts / Q000473:pathology
keywords: comparative oncology; imprinted gene network; parent–offspring conflict; stem cells; trophoblast