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Article: Differential expression of insulin-like growth factor binding protein 1 and ferritin light polypeptide in gestational trophoblastic neoplasia: Combined cDNA suppression subtractive hybridization and microarray study

TitleDifferential expression of insulin-like growth factor binding protein 1 and ferritin light polypeptide in gestational trophoblastic neoplasia: Combined cDNA suppression subtractive hybridization and microarray study
Authors
KeywordscDNA microarray
FTL
Gestational trophoblastic neoplasia
IGFBP1
Suppression subtractive hybridization
Issue Date2005
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741
Citation
Cancer, 2005, v. 104 n. 11, p. 2409-2416 How to Cite?
AbstractBACKGROUND. Hydatidiform mole (HM), the most common type of gestational trophoblastic diseases, can be considered as placenta with abnormal chromosome composition with potential of malignant transformation. Few biologic markers can predict subsequent development of persistent gestational trophoblastic neoplasia (GTN) requiring chemotherapy. METHODS. Suppression subtractive hybridization (SSH) combined with cDNA microarray was used to compare the differential expression pattern of HM that spontaneously regressed and that subsequently developed metastatic GTN. Tissue-specific chips were constructed from the subtracted cDNA libraries, followed by cDNA microarray analysis. Verification by quantitative RNA analysis by real-time polymerase chain reaction (PCR) and immunohistochemical analysis was performed in 23 genotyped complete HM. RESULTS. Sixteen differentially expressed transcripts were identified. Quantitative RNA analysis confirmed down-regulation of ferritin light polypeptide (FTL) (P = 0.037) and insulin-like growth factor binding protein 1 (IGFBP1) (P = 0.037) in HM that subsequently developed GTN when compared with those HM that regressed. Immunohistochemical analysis further confirmed reduced IGFBP1 protein (P = 0.03) expression in HM that developed GTN. CONCLUSIONS. Findings showed that reduced expression of genes related to cell invasion and immunosuppression, especially FTL and IGFBP1, were associated with development of GTN, and this finding may provide a better understanding of the pathogenesis of GTN. The potential application of FTL and IGFBP1 in management of patients with HM should be explored. © 2005 American Cancer Society.
Persistent Identifierhttp://hdl.handle.net/10722/67904
ISSN
2015 Impact Factor: 5.649
2015 SCImago Journal Rankings: 3.188
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFeng, HCen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorNgan, HYSen_HK
dc.contributor.authorXue, WCen_HK
dc.contributor.authorChiu, PMen_HK
dc.contributor.authorCheung, ANYen_HK
dc.date.accessioned2010-09-06T05:59:20Z-
dc.date.available2010-09-06T05:59:20Z-
dc.date.issued2005en_HK
dc.identifier.citationCancer, 2005, v. 104 n. 11, p. 2409-2416en_HK
dc.identifier.issn0008-543Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/67904-
dc.description.abstractBACKGROUND. Hydatidiform mole (HM), the most common type of gestational trophoblastic diseases, can be considered as placenta with abnormal chromosome composition with potential of malignant transformation. Few biologic markers can predict subsequent development of persistent gestational trophoblastic neoplasia (GTN) requiring chemotherapy. METHODS. Suppression subtractive hybridization (SSH) combined with cDNA microarray was used to compare the differential expression pattern of HM that spontaneously regressed and that subsequently developed metastatic GTN. Tissue-specific chips were constructed from the subtracted cDNA libraries, followed by cDNA microarray analysis. Verification by quantitative RNA analysis by real-time polymerase chain reaction (PCR) and immunohistochemical analysis was performed in 23 genotyped complete HM. RESULTS. Sixteen differentially expressed transcripts were identified. Quantitative RNA analysis confirmed down-regulation of ferritin light polypeptide (FTL) (P = 0.037) and insulin-like growth factor binding protein 1 (IGFBP1) (P = 0.037) in HM that subsequently developed GTN when compared with those HM that regressed. Immunohistochemical analysis further confirmed reduced IGFBP1 protein (P = 0.03) expression in HM that developed GTN. CONCLUSIONS. Findings showed that reduced expression of genes related to cell invasion and immunosuppression, especially FTL and IGFBP1, were associated with development of GTN, and this finding may provide a better understanding of the pathogenesis of GTN. The potential application of FTL and IGFBP1 in management of patients with HM should be explored. © 2005 American Cancer Society.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741en_HK
dc.relation.ispartofCanceren_HK
dc.rightsCancer. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectcDNA microarrayen_HK
dc.subjectFTLen_HK
dc.subjectGestational trophoblastic neoplasiaen_HK
dc.subjectIGFBP1en_HK
dc.subjectSuppression subtractive hybridizationen_HK
dc.subject.meshAdolescenten_HK
dc.subject.meshAdulten_HK
dc.subject.meshApoferritinsen_HK
dc.subject.meshDNA, Complementary - geneticsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshFerritinsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIn Situ Hybridization - methodsen_HK
dc.subject.meshInsulin-Like Growth Factor Binding Protein 1 - geneticsen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshOligonucleotide Array Sequence Analysis - methodsen_HK
dc.subject.meshPeptides - geneticsen_HK
dc.subject.meshPolymerase Chain Reactionen_HK
dc.subject.meshPregnancyen_HK
dc.subject.meshPregnancy Complications, Neoplastic - geneticsen_HK
dc.subject.meshTrophoblastic Neoplasms - geneticsen_HK
dc.subject.meshUterine Neoplasms - geneticsen_HK
dc.titleDifferential expression of insulin-like growth factor binding protein 1 and ferritin light polypeptide in gestational trophoblastic neoplasia: Combined cDNA suppression subtractive hybridization and microarray studyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0008-543X&volume=104&issue=11&spage=2409&epage=2416&date=2005&atitle=Differential+expression+of+insulin-like+growth+factor+binding+protein+1+and+ferritin+light+polypeptide+in+gestational+trophoblastic+neoplasia:+combined+cDNA+suppression+subtractive+hybridization+and+microarray+studyen_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailNgan, HYS:hysngan@hkucc.hku.hken_HK
dc.identifier.emailCheung, ANY:anycheun@hkucc.hku.hken_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/cncr.21483en_HK
dc.identifier.pmid16222695-
dc.identifier.scopuseid_2-s2.0-28044446312en_HK
dc.identifier.hkuros109436en_HK
dc.identifier.hkuros130540en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-28044446312&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume104en_HK
dc.identifier.issue11en_HK
dc.identifier.spage2409en_HK
dc.identifier.epage2416en_HK
dc.identifier.isiWOS:000233419200014-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridFeng, HC=7401736336en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK
dc.identifier.scopusauthoridXue, WC=7103165268en_HK
dc.identifier.scopusauthoridChiu, PM=7103182596en_HK
dc.identifier.scopusauthoridCheung, ANY=7401806538en_HK

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