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Article: Clinicopathological roles of alterations of tumor suppressor gene p16 in papillary thyroid carcinoma

TitleClinicopathological roles of alterations of tumor suppressor gene p16 in papillary thyroid carcinoma
Authors
KeywordsExpression
Methylation
p16
Papillary thyroid carcinoma
Issue Date2007
PublisherSpringer New York LLC. The Journal's web site is located at http://www.annalssurgicaloncology.org
Citation
Annals Of Surgical Oncology, 2007, v. 14 n. 5, p. 1772-1779 How to Cite?
AbstractBackground: Alterations of the p16 gene are common in human cancers, but their roles in thyroid cancers have not been clearly defined. The aim of the present study was to investigate the clinicopathological roles of the p16 gene in papillary thyroid carcinoma (PTC). Methods: p16 gene alterations were investigated in 44 patients with PTC (9 men, 35 women) by immunohistochemistry, reverse transcriptase-polymerase chain reaction and methylation-specific polymerase chain reaction. The findings were correlated with their clinicopathological features. Results: p16 protein expression, mRNA alterations, and promoter methylation were detected in 89% (n = 39), 77% (n = 33), and 41% (n = 18) of patients with PTC, respectively. There was no marked relationship between p16 protein expression, mRNA alteration, and promoter methylation. In follicular variant of PTC (FVPTC), there was a frequent lack of p16 protein expression and promoter methylation. PTCs showing p16 promoter methylation were often associated with a high AMES (age, metastasis to distant sites, extrathyroidal invasion, size) risk group and advanced pTNM (tumor-lymph node-metastasis) stages. Conclusions: p16 gene alterations are common and correlate with histological features and biological aggressiveness in PTC, suggesting that they might play an important role in its pathogenesis. © 2006 Society of Surgical Oncology.
Persistent Identifierhttp://hdl.handle.net/10722/172939
ISSN
2021 Impact Factor: 4.339
2020 SCImago Journal Rankings: 1.764
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLam, AKYen_US
dc.contributor.authorLo, CYen_US
dc.contributor.authorLeung, Pen_US
dc.contributor.authorLang, BHHen_US
dc.contributor.authorChan, WFen_US
dc.contributor.authorLuk, JMen_US
dc.date.accessioned2012-10-30T06:25:55Z-
dc.date.available2012-10-30T06:25:55Z-
dc.date.issued2007en_US
dc.identifier.citationAnnals Of Surgical Oncology, 2007, v. 14 n. 5, p. 1772-1779en_US
dc.identifier.issn1068-9265en_US
dc.identifier.urihttp://hdl.handle.net/10722/172939-
dc.description.abstractBackground: Alterations of the p16 gene are common in human cancers, but their roles in thyroid cancers have not been clearly defined. The aim of the present study was to investigate the clinicopathological roles of the p16 gene in papillary thyroid carcinoma (PTC). Methods: p16 gene alterations were investigated in 44 patients with PTC (9 men, 35 women) by immunohistochemistry, reverse transcriptase-polymerase chain reaction and methylation-specific polymerase chain reaction. The findings were correlated with their clinicopathological features. Results: p16 protein expression, mRNA alterations, and promoter methylation were detected in 89% (n = 39), 77% (n = 33), and 41% (n = 18) of patients with PTC, respectively. There was no marked relationship between p16 protein expression, mRNA alteration, and promoter methylation. In follicular variant of PTC (FVPTC), there was a frequent lack of p16 protein expression and promoter methylation. PTCs showing p16 promoter methylation were often associated with a high AMES (age, metastasis to distant sites, extrathyroidal invasion, size) risk group and advanced pTNM (tumor-lymph node-metastasis) stages. Conclusions: p16 gene alterations are common and correlate with histological features and biological aggressiveness in PTC, suggesting that they might play an important role in its pathogenesis. © 2006 Society of Surgical Oncology.en_US
dc.languageengen_US
dc.publisherSpringer New York LLC. The Journal's web site is located at http://www.annalssurgicaloncology.orgen_US
dc.relation.ispartofAnnals of Surgical Oncologyen_US
dc.subjectExpression-
dc.subjectMethylation-
dc.subjectp16-
dc.subjectPapillary thyroid carcinoma-
dc.subject.meshAdenocarcinoma, Follicular - Genetics - Metabolism - Pathologyen_US
dc.subject.meshAdolescenten_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshAged, 80 And Overen_US
dc.subject.meshCarcinoma, Papillary - Genetics - Metabolism - Pathologyen_US
dc.subject.meshChilden_US
dc.subject.meshCyclin-Dependent Kinase Inhibitor P16 - Genetics - Metabolismen_US
dc.subject.meshDna Methylationen_US
dc.subject.meshDna, Neoplasm - Genetics - Metabolismen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunoenzyme Techniquesen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshRna, Messenger - Genetics - Metabolismen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshThyroid Neoplasms - Genetics - Metabolism - Pathologyen_US
dc.titleClinicopathological roles of alterations of tumor suppressor gene p16 in papillary thyroid carcinomaen_US
dc.typeArticleen_US
dc.identifier.emailLuk, JM: jmluk@hkucc.hku.hken_US
dc.identifier.authorityLuk, JM=rp00349en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1245/s10434-006-9280-9en_US
dc.identifier.pmid17195959-
dc.identifier.scopuseid_2-s2.0-34249027956en_US
dc.identifier.hkuros136170-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34249027956&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume14en_US
dc.identifier.issue5en_US
dc.identifier.spage1772en_US
dc.identifier.epage1779en_US
dc.identifier.isiWOS:000246591200035-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLam, AKY=7403657165en_US
dc.identifier.scopusauthoridLo, CY=16417392800en_US
dc.identifier.scopusauthoridLeung, P=7401749062en_US
dc.identifier.scopusauthoridLang, BHH=7201907327en_US
dc.identifier.scopusauthoridChan, WF=16315313900en_US
dc.identifier.scopusauthoridLuk, JM=7006777791en_US
dc.identifier.issnl1068-9265-

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