Hypomethylation and increased gene expression of p16INK4a in primary and metastatic breast carcinoma as compared to normal breast tissue
Controversy continues to surround the role of p16INK4a in cell cycle control and carcinogenesis. Mutations, deletions and changes in methylation patterns of p16INK4a have been proposed as mechanisms leading to abnormal expression of the gene. We show here that primary and metastatic breast carcinoma...
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| Veröffentlicht in: | Oncogene 1998-05, Vol.16 (21), p.2723-2727 |
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| creator | VAN ZEE, K. J CALVANO, J. E BISOGNA, M |
| description | Controversy continues to surround the role of p16INK4a in cell cycle control and carcinogenesis. Mutations, deletions and changes in methylation patterns of p16INK4a have been proposed as mechanisms leading to abnormal expression of the gene. We show here that primary and metastatic breast carcinomas demonstrate hypomethylation of p16INK4a which is associated with expression of p16INK4a mRNA, as compared to normal breast tissue which demonstrates a relative hypermethylation of p16INK4a associated with the absence of p16INK4a expression. These data suggest that methylation and lack of expression of p16INK4a is not a central mechanism in the development of breast carcinoma, but rather that the gene is functioning and expressed in breast carcinoma more frequently than in normal breast tissue. The role of p16INK4a is much more complex than has been previously hypothesized. |
| doi_str_mv | 10.1038/sj.onc.1201794 |
| format | Article |
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The role of p16INK4a is much more complex than has been previously hypothesized.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1201794</identifier><identifier>PMID: 9652738</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing</publisher><subject>Biological and medical sciences ; Breast - metabolism ; Breast - pathology ; Breast cancer ; Breast carcinoma ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Breast Neoplasms - secondary ; Carcinogenesis ; Cell cycle ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Cyclin-Dependent Kinase Inhibitor p16 - genetics ; DNA Methylation ; DNA, Neoplasm - metabolism ; Female ; Fundamental and applied biological sciences. Psychology ; Gene expression ; Gene Expression Regulation, Neoplastic ; Humans ; INK4a protein ; Metastases ; Metastasis ; Molecular and cellular biology ; p16 Protein ; RNA, Messenger ; Tumor Cells, Cultured</subject><ispartof>Oncogene, 1998-05, Vol.16 (21), p.2723-2727</ispartof><rights>1998 INIST-CNRS</rights><rights>Macmillan Publishers Limited 1998.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1948-d5cac05a71606c3fc447ad8db2bc50f3f7de49d9b1dfd5fa3e52eba9e039bb693</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2260587$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9652738$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>VAN ZEE, K. J</creatorcontrib><creatorcontrib>CALVANO, J. E</creatorcontrib><creatorcontrib>BISOGNA, M</creatorcontrib><title>Hypomethylation and increased gene expression of p16INK4a in primary and metastatic breast carcinoma as compared to normal breast tissue</title><title>Oncogene</title><addtitle>Oncogene</addtitle><description>Controversy continues to surround the role of p16INK4a in cell cycle control and carcinogenesis. Mutations, deletions and changes in methylation patterns of p16INK4a have been proposed as mechanisms leading to abnormal expression of the gene. We show here that primary and metastatic breast carcinomas demonstrate hypomethylation of p16INK4a which is associated with expression of p16INK4a mRNA, as compared to normal breast tissue which demonstrates a relative hypermethylation of p16INK4a associated with the absence of p16INK4a expression. These data suggest that methylation and lack of expression of p16INK4a is not a central mechanism in the development of breast carcinoma, but rather that the gene is functioning and expressed in breast carcinoma more frequently than in normal breast tissue. The role of p16INK4a is much more complex than has been previously hypothesized.</description><subject>Biological and medical sciences</subject><subject>Breast - metabolism</subject><subject>Breast - pathology</subject><subject>Breast cancer</subject><subject>Breast carcinoma</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - pathology</subject><subject>Breast Neoplasms - secondary</subject><subject>Carcinogenesis</subject><subject>Cell cycle</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - genetics</subject><subject>DNA Methylation</subject><subject>DNA, Neoplasm - metabolism</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>INK4a protein</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Molecular and cellular biology</subject><subject>p16 Protein</subject><subject>RNA, Messenger</subject><subject>Tumor Cells, Cultured</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kEtP3DAUhS1URIfHtrtKltptpn4m8bJCFFBR2cA6uvGDZjSxU9-M1PkH_Gw8EJAXXpzvfJYPIV84W3Mm2x-4Wado11ww3hh1RFZcNXWltVGfyIoZzSojpPhMThE3jLHGMHFCTkytRSPbFXm-2U9p9PPf_RbmIUUK0dEh2uwBvaNPPnrq_0_ZIx7SFOjE69s_vxUUik55GCHvX0tFAjgXiaX9oT1TC9kOMY1AAalN4wS5KOdEY8ojbN-xeUDc-XNyHGCL_mK5z8jjr6uHy5vq7v769vLnXWW5UW3ltAXLNDS8ZrWVwSrVgGtdL3qrWZChcV4ZZ3rugtMBpNfC92A8k6bvayPPyLc375TTv53HudukXY7lyU7UigtTTluo9Rtlc0LMPnTLVzvOusPuHW66snu37F4KXxftrh-9-8CXoUv-fckBLWxDhmgH_MCEqJluG_kCHAWO1w</recordid><startdate>19980528</startdate><enddate>19980528</enddate><creator>VAN ZEE, K. 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E ; BISOGNA, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1948-d5cac05a71606c3fc447ad8db2bc50f3f7de49d9b1dfd5fa3e52eba9e039bb693</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Biological and medical sciences</topic><topic>Breast - metabolism</topic><topic>Breast - pathology</topic><topic>Breast cancer</topic><topic>Breast carcinoma</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - pathology</topic><topic>Breast Neoplasms - secondary</topic><topic>Carcinogenesis</topic><topic>Cell cycle</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - genetics</topic><topic>DNA Methylation</topic><topic>DNA, Neoplasm - metabolism</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. 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We show here that primary and metastatic breast carcinomas demonstrate hypomethylation of p16INK4a which is associated with expression of p16INK4a mRNA, as compared to normal breast tissue which demonstrates a relative hypermethylation of p16INK4a associated with the absence of p16INK4a expression. These data suggest that methylation and lack of expression of p16INK4a is not a central mechanism in the development of breast carcinoma, but rather that the gene is functioning and expressed in breast carcinoma more frequently than in normal breast tissue. The role of p16INK4a is much more complex than has been previously hypothesized.</abstract><cop>Basingstoke</cop><pub>Nature Publishing</pub><pmid>9652738</pmid><doi>10.1038/sj.onc.1201794</doi><tpages>5</tpages></addata></record> |
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| source | MEDLINE; Nature; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; SpringerLink Journals - AutoHoldings |
| subjects | Biological and medical sciences Breast - metabolism Breast - pathology Breast cancer Breast carcinoma Breast Neoplasms - genetics Breast Neoplasms - pathology Breast Neoplasms - secondary Carcinogenesis Cell cycle Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cyclin-Dependent Kinase Inhibitor p16 - genetics DNA Methylation DNA, Neoplasm - metabolism Female Fundamental and applied biological sciences. Psychology Gene expression Gene Expression Regulation, Neoplastic Humans INK4a protein Metastases Metastasis Molecular and cellular biology p16 Protein RNA, Messenger Tumor Cells, Cultured |
| title | Hypomethylation and increased gene expression of p16INK4a in primary and metastatic breast carcinoma as compared to normal breast tissue |
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