Fibroblast subpopulations as accelerators of tumor progression: the role of migration stimulating factor.
Tumor progression is a relatively indolent process, with many years commonly intervening between the inception of an initiating genetic lesion and the development of overt malignant disease. We suggest that the perturbation of normal epithelial-mesenchymal interactions caused by the inappropriate presence of fibroblast subpopulations displaying various 'fetal-like' phenotypic characteristics may significantly alter the kinetics of tumor progression and hence enhance susceptibility to cancer development. In this communication, we review our own data indicating the presence of fetal-like fibroblasts in cancer patients and put these observations in the context of similar published reports. We then discuss our interpretation of these findings, emphasising the possible direct involvement of fetal-like fibroblasts in cancer pathogenesis and putting forward an epigenetic 'clonal modulation' model to account for their presence in cancer patients.
Department of Dental Surgery and Periodontology, Dental School, University of Dundee, Scotland, UK.
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Schor
D000328:Adult; D000818:Animals; D002465:Cell Movement; D002471:Cell Transformation, Neoplastic; D016207:Cytokines / Q000502:physiology*; D005333:Fetus; D005347:Fibroblasts / Q000166:cytology / Q000473:pathology / Q000502:physiology; D005353:Fibronectins; D006801:Humans; D009369:Neoplasms / Q000473:pathology* / Q000503:physiopathology*; D010641:Phenotype; D012016:Reference Values
D016207:Cytokines; C067625:FN1 protein, human; D005353:Fibronectins