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dc.contributor.authorSchor, Seth L
dc.contributor.authorSchor, Ana M
dc.contributor.authorHowell, Anthony
dc.contributor.authorCrowther, Derek
dc.date.accessioned2010-10-20T08:44:51Z
dc.date.available2010-10-20T08:44:51Z
dc.date.issued1987
dc.identifier.citationHypothesis: persistent expression of fetal phenotypic characteristics by fibroblasts is associated with an increased susceptibility to neoplastic disease. 1987, 55 (1):11-7 Exp. Cell Biol.en
dc.identifier.issn0304-3568
dc.identifier.pmid3569635
dc.identifier.doi10.1159/000163389
dc.identifier.urihttp://hdl.handle.net/10541/113527
dc.description.abstractPublished data from our own and other laboratories have indicated that fibroblasts obtained from patients with different types of epithelial cancers commonly display aberrant (i.e. fetal-like or transformed) phenotypic characteristics. Previous interpretations of these results have tended to regard the study of fibroblasts as a convenient means to demonstrate genetic abnormalities also expressed in the target epithelial cell population and did not ascribe a particular causative role to fibroblast abnormalities in the genesis of neoplastic lesions. In this communication we present an alternative, but not mutually exclusive, hypothesis suggesting that aberrations expressed solely by fibroblasts may lead to the development of an epithelial tumour by virtue of a dysfunction in normal epithelial-mesenchymal interactions.
dc.language.isoenen
dc.subjectFoetusen
dc.subjectCanceren
dc.subject.meshDisease Susceptibility
dc.subject.meshFetus
dc.subject.meshFibroblasts
dc.subject.meshHumans
dc.subject.meshNeoplasms
dc.subject.meshPhenotype
dc.titleHypothesis: persistent expression of fetal phenotypic characteristics by fibroblasts is associated with an increased susceptibility to neoplastic disease.en
dc.typeArticleen
dc.identifier.journalExperimental Cell Biologyen
html.description.abstractPublished data from our own and other laboratories have indicated that fibroblasts obtained from patients with different types of epithelial cancers commonly display aberrant (i.e. fetal-like or transformed) phenotypic characteristics. Previous interpretations of these results have tended to regard the study of fibroblasts as a convenient means to demonstrate genetic abnormalities also expressed in the target epithelial cell population and did not ascribe a particular causative role to fibroblast abnormalities in the genesis of neoplastic lesions. In this communication we present an alternative, but not mutually exclusive, hypothesis suggesting that aberrations expressed solely by fibroblasts may lead to the development of an epithelial tumour by virtue of a dysfunction in normal epithelial-mesenchymal interactions.


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