File Download
Supplementary

postgraduate thesis: The role of FoxD3 in gestational trophoblastic disease

TitleThe role of FoxD3 in gestational trophoblastic disease
Authors
Issue Date2012
PublisherThe University of Hong Kong (Pokfulam, Hong Kong)
AbstractGestational trophoblastic disease (GTD) is arised from the neoplastic trophoblasts in placenta. Trophoblasts have the characteristic of proliferation and invasion. GTD is classified as partial hydatidiform mole (PHM), complete hydatidiform form mole (CHM), invasive hydatidiform mole (IHM), choriocarcinoma (CCA), placental site trophoblastic tumour (PSTT), epithelioid trophoblastic tumour (ETT), exaggerated placental site trophoblastic reaction (EPSR) and placental site nodule (PSN). HM has the potential to develop into malignant trophoblastic disease, and metastasis to other parts of body. FoxD3 gene belongs to Forkhead family. Its protein acts as embryonic stem cell transcription factor and plays an important role in neural crest and placenta development. Previous studies from our team have reported that other embryonic stem cell transcription factors, such as Nanog, Sox2 Oct4 and Stat3, are related with pathogenesis of GTD. This study aim is to investigate the protein expression profile of FoxD3 in different types of GTD using immunohistochemistry method. In this study, 70 formalin fixed paraffin embedded tissue blocks from 16 normal first trimester placenta, 38 CHM, 9 CCA, 5 PSTT and 2 ETT were retrieved. Paraffin sections were prepared and stained with FoxD3 antibody by using immunohistochemistry method. Compared with normal placentas, there was significantly increased expression of FoxD3 in trophoblasts of CM and PSTT (p<0.05). In CCA, there was high expression of FoxD3 in syncytiotrophoblasts and intermediate trophoblasts (p<0.05). In ETT, the immunoreactivity of FoxD3 is not significantly increased when compared with intermediate trophoblasts (p=0.07). To conclude, FoxD3 was found to be over-expressed in GTD. FoxD3 may contribute to pathogenesis of GTD. Further investigations are needed to discover the relationship with other embryonic transcription factors and genes to improve the diagnosis, prognosis and treatment of GTD.
DegreeMaster of Medical Sciences
SubjectTrophoblastic tumors.
Transcription factors.
Dept/ProgramPathology

 

DC FieldValueLanguage
dc.contributor.authorChiu, Ka-yue.-
dc.contributor.author招家裕.-
dc.date.issued2012-
dc.description.abstractGestational trophoblastic disease (GTD) is arised from the neoplastic trophoblasts in placenta. Trophoblasts have the characteristic of proliferation and invasion. GTD is classified as partial hydatidiform mole (PHM), complete hydatidiform form mole (CHM), invasive hydatidiform mole (IHM), choriocarcinoma (CCA), placental site trophoblastic tumour (PSTT), epithelioid trophoblastic tumour (ETT), exaggerated placental site trophoblastic reaction (EPSR) and placental site nodule (PSN). HM has the potential to develop into malignant trophoblastic disease, and metastasis to other parts of body. FoxD3 gene belongs to Forkhead family. Its protein acts as embryonic stem cell transcription factor and plays an important role in neural crest and placenta development. Previous studies from our team have reported that other embryonic stem cell transcription factors, such as Nanog, Sox2 Oct4 and Stat3, are related with pathogenesis of GTD. This study aim is to investigate the protein expression profile of FoxD3 in different types of GTD using immunohistochemistry method. In this study, 70 formalin fixed paraffin embedded tissue blocks from 16 normal first trimester placenta, 38 CHM, 9 CCA, 5 PSTT and 2 ETT were retrieved. Paraffin sections were prepared and stained with FoxD3 antibody by using immunohistochemistry method. Compared with normal placentas, there was significantly increased expression of FoxD3 in trophoblasts of CM and PSTT (p<0.05). In CCA, there was high expression of FoxD3 in syncytiotrophoblasts and intermediate trophoblasts (p<0.05). In ETT, the immunoreactivity of FoxD3 is not significantly increased when compared with intermediate trophoblasts (p=0.07). To conclude, FoxD3 was found to be over-expressed in GTD. FoxD3 may contribute to pathogenesis of GTD. Further investigations are needed to discover the relationship with other embryonic transcription factors and genes to improve the diagnosis, prognosis and treatment of GTD.-
dc.languageeng-
dc.publisherThe University of Hong Kong (Pokfulam, Hong Kong)-
dc.relation.ispartofHKU Theses Online (HKUTO)-
dc.rightsThe author retains all proprietary rights, (such as patent rights) and the right to use in future works.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.source.urihttp://hub.hku.hk/bib/B48333633-
dc.subject.lcshTrophoblastic tumors.-
dc.subject.lcshTranscription factors.-
dc.titleThe role of FoxD3 in gestational trophoblastic disease-
dc.typePG_Thesis-
dc.identifier.hkulb4833363-
dc.description.thesisnameMaster of Medical Sciences-
dc.description.thesislevelMaster-
dc.description.thesisdisciplinePathology-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.5353/th_b4833363-
dc.date.hkucongregation2012-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats