Fetal diagnosis and therapy · 2006
The changes in angiogenic gene expression in recurrent multiple chorioangiomas.
Клинический случайСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Gallot Denis, Marceau Geoffroy, Laurichesse-Delmas Hélène, Vanlieferinghen Philippe, Dechelotte Pierre J, Lemery Didier, Sapin Vincent
Аннотация
OBJECTIVES: To assess the messenger ribonucleic acid expression in placental tissue of growth factors, cytokines, angiogenic and anti-angiogenic factors in one case of recurrent multiple chorioangiomas.
METHODS: Complementary deoxyribonucleic acid array analysis was performed on the affected placentae and on normal placentaes (controls) to compare messenger ribonucleic acid levels of 96 genes involved in angiogenesis.
RESULTS: Eleven genes presented more than two-fold alteration in expression levels: undetectable (angiopoietin 1, osteonectin, tyrosine kinase endothelial, neuropilin 1), decreased (transcription growth factor beta receptor 3, tissue inhibitor of metalloproteinase type 2, EGF receptor, integrin-alpha V, tyrosine kinase vascular endothelial growth factor receptor 2), increased (angiopoietin 2, osteopontin).
CONCLUSIONS: We illustrated the complexity of angiogenic disruption in recurrent multiple chorioangiomas leading to the difficulty to propose a single candidate gene to explain this pathology.
METHODS: Complementary deoxyribonucleic acid array analysis was performed on the affected placentae and on normal placentaes (controls) to compare messenger ribonucleic acid levels of 96 genes involved in angiogenesis.
RESULTS: Eleven genes presented more than two-fold alteration in expression levels: undetectable (angiopoietin 1, osteonectin, tyrosine kinase endothelial, neuropilin 1), decreased (transcription growth factor beta receptor 3, tissue inhibitor of metalloproteinase type 2, EGF receptor, integrin-alpha V, tyrosine kinase vascular endothelial growth factor receptor 2), increased (angiopoietin 2, osteopontin).
CONCLUSIONS: We illustrated the complexity of angiogenic disruption in recurrent multiple chorioangiomas leading to the difficulty to propose a single candidate gene to explain this pathology.