Clinicopathological roles of alterations of tumor suppressor gene p16 in papillary thyroid carcinoma
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). p16 gene alterations were investigated in 44...
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| Veröffentlicht in: | Annals of surgical oncology 2007-05, Vol.14 (5), p.1772-1779 |
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| creator | Lam, Alfred King Yin Lo, Chung Yau Leung, Pauline Lang, Brian Hung Hin Chan, Wai Fun Luk, John M |
| description | 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).
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.
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.
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. |
| doi_str_mv | 10.1245/s10434-006-9280-9 |
| format | Article |
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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.
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.
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.</description><identifier>ISSN: 1068-9265</identifier><identifier>EISSN: 1534-4681</identifier><identifier>DOI: 10.1245/s10434-006-9280-9</identifier><identifier>PMID: 17195959</identifier><language>eng</language><publisher>United States: Springer Nature B.V</publisher><subject>Adenocarcinoma, Follicular - genetics ; Adenocarcinoma, Follicular - metabolism ; Adenocarcinoma, Follicular - pathology ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Carcinoma, Papillary - genetics ; Carcinoma, Papillary - metabolism ; Carcinoma, Papillary - pathology ; Child ; Cyclin-Dependent Kinase Inhibitor p16 - genetics ; Cyclin-Dependent Kinase Inhibitor p16 - metabolism ; DNA Methylation ; DNA, Neoplasm - genetics ; DNA, Neoplasm - metabolism ; Female ; Gene expression ; Humans ; Immunoenzyme Techniques ; Immunohistochemistry ; Lymph nodes ; Male ; Metastases ; Metastasis ; Middle Aged ; p16 Protein ; Papillary thyroid carcinoma ; Polymerase chain reaction ; Promoter Regions, Genetic ; Protein expression ; Proteins ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; RNA-directed DNA polymerase ; Thyroid ; Thyroid cancer ; Thyroid Neoplasms - genetics ; Thyroid Neoplasms - metabolism ; Thyroid Neoplasms - pathology ; Tumor suppressor genes ; Tumors</subject><ispartof>Annals of surgical oncology, 2007-05, Vol.14 (5), p.1772-1779</ispartof><rights>Society of Surgical Oncology 2007</rights><rights>Society of Surgical Oncology 2006.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-5527d2fe3fde8532fb08626001ac0984b045acf113f14f79e51cbd33485348073</citedby><cites>FETCH-LOGICAL-c420t-5527d2fe3fde8532fb08626001ac0984b045acf113f14f79e51cbd33485348073</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17195959$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lam, Alfred King Yin</creatorcontrib><creatorcontrib>Lo, Chung Yau</creatorcontrib><creatorcontrib>Leung, Pauline</creatorcontrib><creatorcontrib>Lang, Brian Hung Hin</creatorcontrib><creatorcontrib>Chan, Wai Fun</creatorcontrib><creatorcontrib>Luk, John M</creatorcontrib><title>Clinicopathological roles of alterations of tumor suppressor gene p16 in papillary thyroid carcinoma</title><title>Annals of surgical oncology</title><addtitle>Ann Surg Oncol</addtitle><description>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).
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.
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.
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.</description><subject>Adenocarcinoma, Follicular - genetics</subject><subject>Adenocarcinoma, Follicular - metabolism</subject><subject>Adenocarcinoma, Follicular - pathology</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Carcinoma, Papillary - genetics</subject><subject>Carcinoma, Papillary - metabolism</subject><subject>Carcinoma, Papillary - pathology</subject><subject>Child</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - genetics</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - metabolism</subject><subject>DNA Methylation</subject><subject>DNA, Neoplasm - genetics</subject><subject>DNA, Neoplasm - metabolism</subject><subject>Female</subject><subject>Gene expression</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>Immunohistochemistry</subject><subject>Lymph nodes</subject><subject>Male</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Middle Aged</subject><subject>p16 Protein</subject><subject>Papillary thyroid carcinoma</subject><subject>Polymerase chain reaction</subject><subject>Promoter Regions, Genetic</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA-directed DNA polymerase</subject><subject>Thyroid</subject><subject>Thyroid cancer</subject><subject>Thyroid Neoplasms - genetics</subject><subject>Thyroid Neoplasms - metabolism</subject><subject>Thyroid Neoplasms - pathology</subject><subject>Tumor suppressor genes</subject><subject>Tumors</subject><issn>1068-9265</issn><issn>1534-4681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kUtr3TAQRkVpaZ4_oJsiGsjO6YzeXpZL-oBANu1a6MpSomBbrmQv8u-j9F4oFIoWGklnhg8dQj4g3CAT8nNFEFx0AKrrmYGuf0NOUbYboQy-bTUo016UPCFntT4BoOYg35MT1NjLtk7JsBvTnHxe3PqYx_yQvBtpyWOoNEfqxjUUt6Y8_zmu25QLrduylFBrKx_CHOiCiqaZLm5J4-jKM10fn0tOA_Wu-DTnyV2Qd9GNNVwe93Py6-vtz9337u7-24_dl7vOCwZrJyXTA4uBxyEYyVncg1FMtdjOQ2_EHoR0PiLyiCLqPkj0-4Fz0WBhQPNzcn2Yu5T8ewt1tVOqPrRUc8hbtRokA2NMA6_-AZ_yVuaWzTKlJDdgtGrUp_9STHNtUGCD8AD5kmstIdqlpKl9g0Wwr5bswZJtluyrJdu3no_Hwdt-CsPfjqMW_gKAeoyG</recordid><startdate>20070501</startdate><enddate>20070501</enddate><creator>Lam, Alfred King Yin</creator><creator>Lo, Chung Yau</creator><creator>Leung, Pauline</creator><creator>Lang, Brian Hung Hin</creator><creator>Chan, Wai Fun</creator><creator>Luk, John M</creator><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20070501</creationdate><title>Clinicopathological roles of alterations of tumor suppressor gene p16 in papillary thyroid carcinoma</title><author>Lam, Alfred King Yin ; Lo, Chung Yau ; Leung, Pauline ; Lang, Brian Hung Hin ; Chan, Wai Fun ; Luk, John M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-5527d2fe3fde8532fb08626001ac0984b045acf113f14f79e51cbd33485348073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adenocarcinoma, Follicular - genetics</topic><topic>Adenocarcinoma, Follicular - metabolism</topic><topic>Adenocarcinoma, Follicular - pathology</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Carcinoma, Papillary - genetics</topic><topic>Carcinoma, Papillary - metabolism</topic><topic>Carcinoma, Papillary - pathology</topic><topic>Child</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - genetics</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - metabolism</topic><topic>DNA Methylation</topic><topic>DNA, Neoplasm - genetics</topic><topic>DNA, Neoplasm - metabolism</topic><topic>Female</topic><topic>Gene expression</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>Immunohistochemistry</topic><topic>Lymph nodes</topic><topic>Male</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Middle Aged</topic><topic>p16 Protein</topic><topic>Papillary thyroid carcinoma</topic><topic>Polymerase chain reaction</topic><topic>Promoter Regions, Genetic</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA-directed DNA polymerase</topic><topic>Thyroid</topic><topic>Thyroid cancer</topic><topic>Thyroid Neoplasms - genetics</topic><topic>Thyroid Neoplasms - metabolism</topic><topic>Thyroid Neoplasms - pathology</topic><topic>Tumor suppressor genes</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lam, Alfred King Yin</creatorcontrib><creatorcontrib>Lo, Chung Yau</creatorcontrib><creatorcontrib>Leung, Pauline</creatorcontrib><creatorcontrib>Lang, Brian Hung Hin</creatorcontrib><creatorcontrib>Chan, Wai Fun</creatorcontrib><creatorcontrib>Luk, John M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Annals of surgical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lam, Alfred King Yin</au><au>Lo, Chung Yau</au><au>Leung, Pauline</au><au>Lang, Brian Hung Hin</au><au>Chan, Wai Fun</au><au>Luk, John M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clinicopathological roles of alterations of tumor suppressor gene p16 in papillary thyroid carcinoma</atitle><jtitle>Annals of surgical oncology</jtitle><addtitle>Ann Surg Oncol</addtitle><date>2007-05-01</date><risdate>2007</risdate><volume>14</volume><issue>5</issue><spage>1772</spage><epage>1779</epage><pages>1772-1779</pages><issn>1068-9265</issn><eissn>1534-4681</eissn><abstract>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).
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.
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.
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.</abstract><cop>United States</cop><pub>Springer Nature B.V</pub><pmid>17195959</pmid><doi>10.1245/s10434-006-9280-9</doi><tpages>8</tpages></addata></record> |
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| ispartof | Annals of surgical oncology, 2007-05, Vol.14 (5), p.1772-1779 |
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| subjects | Adenocarcinoma, Follicular - genetics Adenocarcinoma, Follicular - metabolism Adenocarcinoma, Follicular - pathology Adolescent Adult Aged Aged, 80 and over Carcinoma, Papillary - genetics Carcinoma, Papillary - metabolism Carcinoma, Papillary - pathology Child Cyclin-Dependent Kinase Inhibitor p16 - genetics Cyclin-Dependent Kinase Inhibitor p16 - metabolism DNA Methylation DNA, Neoplasm - genetics DNA, Neoplasm - metabolism Female Gene expression Humans Immunoenzyme Techniques Immunohistochemistry Lymph nodes Male Metastases Metastasis Middle Aged p16 Protein Papillary thyroid carcinoma Polymerase chain reaction Promoter Regions, Genetic Protein expression Proteins Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics RNA, Messenger - metabolism RNA-directed DNA polymerase Thyroid Thyroid cancer Thyroid Neoplasms - genetics Thyroid Neoplasms - metabolism Thyroid Neoplasms - pathology Tumor suppressor genes Tumors |
| title | Clinicopathological roles of alterations of tumor suppressor gene p16 in papillary thyroid carcinoma |
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