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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
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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
 
AuthorsFeng, HC1
Tsao, SW1
Ngan, HYS1
Xue, WC1
Chiu, PM1
Cheung, ANY1
 
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
 
CitationCancer, 2005, v. 104 n. 11, p. 2409-2416 [How to Cite?]
DOI: http://dx.doi.org/10.1002/cncr.21483
 
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.
 
ISSN0008-543X
2012 Impact Factor: 5.201
2012 SCImago Journal Rankings: 2.407
 
DOIhttp://dx.doi.org/10.1002/cncr.21483
 
ISI Accession Number IDWOS:000233419200014
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorFeng, HC
 
dc.contributor.authorTsao, SW
 
dc.contributor.authorNgan, HYS
 
dc.contributor.authorXue, WC
 
dc.contributor.authorChiu, PM
 
dc.contributor.authorCheung, ANY
 
dc.date.accessioned2010-09-06T05:59:20Z
 
dc.date.available2010-09-06T05:59:20Z
 
dc.date.issued2005
 
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.
 
dc.description.naturelink_to_OA_fulltext
 
dc.identifier.citationCancer, 2005, v. 104 n. 11, p. 2409-2416 [How to Cite?]
DOI: http://dx.doi.org/10.1002/cncr.21483
 
dc.identifier.doihttp://dx.doi.org/10.1002/cncr.21483
 
dc.identifier.epage2416
 
dc.identifier.hkuros109436
 
dc.identifier.hkuros130540
 
dc.identifier.isiWOS:000233419200014
 
dc.identifier.issn0008-543X
2012 Impact Factor: 5.201
2012 SCImago Journal Rankings: 2.407
 
dc.identifier.issue11
 
dc.identifier.openurl
 
dc.identifier.pmid16222695
 
dc.identifier.scopuseid_2-s2.0-28044446312
 
dc.identifier.spage2409
 
dc.identifier.urihttp://hdl.handle.net/10722/67904
 
dc.identifier.volume104
 
dc.languageeng
 
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741
 
dc.publisher.placeUnited States
 
dc.relation.ispartofCancer
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCancer. Copyright © John Wiley & Sons, Inc.
 
dc.subject.meshAdolescent
 
dc.subject.meshAdult
 
dc.subject.meshApoferritins
 
dc.subject.meshDNA, Complementary - genetics
 
dc.subject.meshFemale
 
dc.subject.meshFerritins
 
dc.subject.meshHumans
 
dc.subject.meshIn Situ Hybridization - methods
 
dc.subject.meshInsulin-Like Growth Factor Binding Protein 1 - genetics
 
dc.subject.meshMiddle Aged
 
dc.subject.meshOligonucleotide Array Sequence Analysis - methods
 
dc.subject.meshPeptides - genetics
 
dc.subject.meshPolymerase Chain Reaction
 
dc.subject.meshPregnancy
 
dc.subject.meshPregnancy Complications, Neoplastic - genetics
 
dc.subject.meshTrophoblastic Neoplasms - genetics
 
dc.subject.meshUterine Neoplasms - genetics
 
dc.subjectcDNA microarray
 
dc.subjectFTL
 
dc.subjectGestational trophoblastic neoplasia
 
dc.subjectIGFBP1
 
dc.subjectSuppression subtractive hybridization
 
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 study
 
dc.typeArticle
 
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<description.abstract>BACKGROUND. 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. &#169; 2005 American Cancer Society.</description.abstract>
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<subject.mesh>Adolescent</subject.mesh>
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Author Affiliations
  1. The University of Hong Kong