Linked Life Data

10065942

Source:http://linkedlifedata.com/resource/pubmed/id/10065942

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-3-8
pubmed:abstractText
Comparative investigations of odontogenic cells in normally forming teeth and tumors may provide insights into the mechanisms of the differentiation process. The present study is devoted to late phenotypic markers of ameloblast and odontoblast cells, i.e., proteins involved in biomineralization. The in situ expression of amelogenins, keratins, collagens type III and IV, vimentin, fibronectin, osteonectin, and osteocalcin was performed on normal and tumor odontogenic human cells. The pattern of protein expression showed some similarities between ameloblasts and odontoblasts present in normally developing human teeth and cells present in neoplastic tissues of ameloblastic fibroma, ameloblastic fibro-odontomas, and complex odontomas. Amelogenins (for ameloblasts) and osteocalcin (for odontoblasts) were detected in cells with well-organized enamel and dentin, respectively. In contrast, "mixed" cells located in epithelial zones of mixed odontogenic tumors co-expressed amelogenins and osteocalcin, as shown by immunostaining. The presence of osteocalcin transcripts was also demonstrated by in situ hybridization in these cells. Keratins and vimentin were detected in the same epithelial zones. Tumor epithelial cells were associated with various amounts of polymorphic matrix (amelogenin- and osteocalcin-immunoreactive), depending on the types of mixed tumors. No osteocalcin labeling was found in epithelial tumors. This study confirms that the differentiation of normal and tumor odontogenic cells is accompanied by the expression of some common molecules. Furthermore, the gene products present in normal mesenchymal cells were also shown in odontogenic tumor epithelium. These data may be related to a tumor-specific overexpression of the corresponding genes transcribed at an undetectable level during normal development and/or to an epithelial-mesenchymal transition proposed to occur during normal root formation. A plausible explanation for the results is that the odontogenic tumor epithelial cells are recapitulating genetic programs expressed during normal odontogenesis, but the tumor cells demonstrate abnormal expression patterns for these genes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
D
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-0345
pubmed:author
pubmed:issnType
Print
pubmed:volume
78
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
20-30
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10065942-Ameloblastoma, pubmed-meshheading:10065942-Amelogenin, pubmed-meshheading:10065942-Cell Differentiation, pubmed-meshheading:10065942-Cell Polarity, pubmed-meshheading:10065942-Cell Transformation, Neoplastic, pubmed-meshheading:10065942-Dental Enamel Proteins, pubmed-meshheading:10065942-Epithelial Cells, pubmed-meshheading:10065942-Extracellular Matrix Proteins, pubmed-meshheading:10065942-Gene Expression Regulation, Developmental, pubmed-meshheading:10065942-Gene Expression Regulation, Neoplastic, pubmed-meshheading:10065942-Humans, pubmed-meshheading:10065942-Immunohistochemistry, pubmed-meshheading:10065942-In Situ Hybridization, pubmed-meshheading:10065942-Infant, Newborn, pubmed-meshheading:10065942-Keratins, pubmed-meshheading:10065942-Odontogenesis, pubmed-meshheading:10065942-Odontogenic Tumors, pubmed-meshheading:10065942-Odontoma, pubmed-meshheading:10065942-Osteocalcin, pubmed-meshheading:10065942-Osteonectin, pubmed-meshheading:10065942-Tumor Cells, Cultured, pubmed-meshheading:10065942-Vimentin
pubmed:year
1999
pubmed:articleTitle
Aberrant gene expression in epithelial cells of mixed odontogenic tumors.
pubmed:affiliation
Laboratoire de Biologie-Odontologie, Institut Biomédical des Cordeliers, Université Paris VII, France.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't