The p16 and p18 tumor suppressor genes in neuroblastoma: implications for drug resistance
The cyclin dependent kinase inhibitors p16 and p18 were investigated in neuroblastoma. Only one of 19 neuroblastoma cell lines, an adriamycin-resistant variant, and none of 5 primary neuroblastoma, was deleted for p16 while its parental drug sensitive cell line is p16 intact. The region of deletion...
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| Veröffentlicht in: | Cancer letters 1996-07, Vol.104 (2), p.183-192 |
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| creator | Diccianni, Mitchell B. Chau, Lan S. Batova, Ayse Vu, Thai Q. Yu, Alice L. |
| description | The cyclin dependent kinase inhibitors p16 and p18 were investigated in neuroblastoma. Only one of 19 neuroblastoma cell lines, an adriamycin-resistant variant, and none of 5 primary neuroblastoma, was deleted for p16 while its parental drug sensitive cell line is p16 intact. The region of deletion minimally extended centromeric to include p15, and telomeric to interferon-β. This is the first report of a p16 gene alteration in neuroblastoma. No p16 gene hypermethylation or mutations were found. No homozygous deletions of p18 in these samples were found, although several instances of loss of heterozygosity are suspected. No p18 point mutations were detected. We conclude that (1) neither p16 nor p18 are likely involved in the pathogenesis of neuroblastoma; and (2) the role of p16, or another 9p21 gene, in the development of drug resistance warrants further investigation. |
| doi_str_mv | 10.1016/0304-3835(96)04250-4 |
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Only one of 19 neuroblastoma cell lines, an adriamycin-resistant variant, and none of 5 primary neuroblastoma, was deleted for p16 while its parental drug sensitive cell line is p16 intact. The region of deletion minimally extended centromeric to include p15, and telomeric to interferon-β. This is the first report of a p16 gene alteration in neuroblastoma. No p16 gene hypermethylation or mutations were found. No homozygous deletions of p18 in these samples were found, although several instances of loss of heterozygosity are suspected. No p18 point mutations were detected. We conclude that (1) neither p16 nor p18 are likely involved in the pathogenesis of neuroblastoma; and (2) the role of p16, or another 9p21 gene, in the development of drug resistance warrants further investigation.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/0304-3835(96)04250-4</identifier><identifier>PMID: 8665486</identifier><identifier>CODEN: CALEDQ</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Antineoplastic agents ; Base Sequence ; Biological and medical sciences ; Carrier Proteins - genetics ; Cell Cycle Proteins ; Chemotherapy ; Chromosome Deletion ; Chromosome Mapping ; Chromosomes, Human, Pair 9 ; Cyclin-dependent kinase inhibitor ; Cyclin-Dependent Kinase Inhibitor p16 ; Cyclin-Dependent Kinase Inhibitor p18 ; Enzyme Inhibitors ; Genes, Tumor Suppressor ; Humans ; Hypermethylation ; Medical sciences ; Molecular Sequence Data ; Neuroblastoma ; Neuroblastoma - genetics ; Neurology ; p16 ; p18 ; Pharmacology. Drug treatments ; Protein Kinase Inhibitors ; Tumor Cells, Cultured ; Tumor Suppressor Proteins ; Tumors of the nervous system. Phacomatoses</subject><ispartof>Cancer letters, 1996-07, Vol.104 (2), p.183-192</ispartof><rights>1996</rights><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c386t-582acc42f1156928154cc1b4e758bbda0d3202b695c5a783a21ae921044ce7a03</citedby><cites>FETCH-LOGICAL-c386t-582acc42f1156928154cc1b4e758bbda0d3202b695c5a783a21ae921044ce7a03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0304-3835(96)04250-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3116960$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8665486$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Diccianni, Mitchell B.</creatorcontrib><creatorcontrib>Chau, Lan S.</creatorcontrib><creatorcontrib>Batova, Ayse</creatorcontrib><creatorcontrib>Vu, Thai Q.</creatorcontrib><creatorcontrib>Yu, Alice L.</creatorcontrib><title>The p16 and p18 tumor suppressor genes in neuroblastoma: implications for drug resistance</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>The cyclin dependent kinase inhibitors p16 and p18 were investigated in neuroblastoma. Only one of 19 neuroblastoma cell lines, an adriamycin-resistant variant, and none of 5 primary neuroblastoma, was deleted for p16 while its parental drug sensitive cell line is p16 intact. The region of deletion minimally extended centromeric to include p15, and telomeric to interferon-β. This is the first report of a p16 gene alteration in neuroblastoma. No p16 gene hypermethylation or mutations were found. No homozygous deletions of p18 in these samples were found, although several instances of loss of heterozygosity are suspected. No p18 point mutations were detected. We conclude that (1) neither p16 nor p18 are likely involved in the pathogenesis of neuroblastoma; and (2) the role of p16, or another 9p21 gene, in the development of drug resistance warrants further investigation.</description><subject>Antineoplastic agents</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Carrier Proteins - genetics</subject><subject>Cell Cycle Proteins</subject><subject>Chemotherapy</subject><subject>Chromosome Deletion</subject><subject>Chromosome Mapping</subject><subject>Chromosomes, Human, Pair 9</subject><subject>Cyclin-dependent kinase inhibitor</subject><subject>Cyclin-Dependent Kinase Inhibitor p16</subject><subject>Cyclin-Dependent Kinase Inhibitor p18</subject><subject>Enzyme Inhibitors</subject><subject>Genes, Tumor Suppressor</subject><subject>Humans</subject><subject>Hypermethylation</subject><subject>Medical sciences</subject><subject>Molecular Sequence Data</subject><subject>Neuroblastoma</subject><subject>Neuroblastoma - genetics</subject><subject>Neurology</subject><subject>p16</subject><subject>p18</subject><subject>Pharmacology. Drug treatments</subject><subject>Protein Kinase Inhibitors</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Suppressor Proteins</subject><subject>Tumors of the nervous system. Phacomatoses</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1r3DAQhkVJSDdp_0EDOoTSHpzq23IOhbKkSSCQS3LoScjyOFHxVzR2of8-MrvsMaeRmOcdZh5CvnB2yRk3P5hkqpBW6m-V-c6U0KxQH8iG21IUZWXZEdkckI_kFPEvY0yrUp-QE2uMVtZsyJ_HF6ATN9QPTa6Wzks_JorLNCVAzM9nGABpHOgASxrrzuM89v6Kxn7qYvBzHAekbQabtDzTHIo4-yHAJ3Lc-g7h876ekaff14_b2-L-4eZu--u-CNKaudBW-BCUaDnXphKWaxUCrxWU2tZ141kjBRO1qXTQvrTSC-6hEpwpFaD0TJ6Rr7u5UxpfF8DZ9REDdJ0fYFzQlZaLUkuTQbUDQxoRE7RuSrH36b_jzK1G3arLrbpclT-rUady7Hw_f6l7aA6hvcLcv9j3PQbftSkfH_GASc5NZdY1f-4wyC7-RUgOQ4TsqYkJwuyaMb6_xxv5DJEj</recordid><startdate>19960712</startdate><enddate>19960712</enddate><creator>Diccianni, Mitchell B.</creator><creator>Chau, Lan S.</creator><creator>Batova, Ayse</creator><creator>Vu, Thai Q.</creator><creator>Yu, Alice L.</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>19960712</creationdate><title>The p16 and p18 tumor suppressor genes in neuroblastoma: implications for drug resistance</title><author>Diccianni, Mitchell B. ; Chau, Lan S. ; Batova, Ayse ; Vu, Thai Q. ; Yu, Alice L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c386t-582acc42f1156928154cc1b4e758bbda0d3202b695c5a783a21ae921044ce7a03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Antineoplastic agents</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Carrier Proteins - genetics</topic><topic>Cell Cycle Proteins</topic><topic>Chemotherapy</topic><topic>Chromosome Deletion</topic><topic>Chromosome Mapping</topic><topic>Chromosomes, Human, Pair 9</topic><topic>Cyclin-dependent kinase inhibitor</topic><topic>Cyclin-Dependent Kinase Inhibitor p16</topic><topic>Cyclin-Dependent Kinase Inhibitor p18</topic><topic>Enzyme Inhibitors</topic><topic>Genes, Tumor Suppressor</topic><topic>Humans</topic><topic>Hypermethylation</topic><topic>Medical sciences</topic><topic>Molecular Sequence Data</topic><topic>Neuroblastoma</topic><topic>Neuroblastoma - genetics</topic><topic>Neurology</topic><topic>p16</topic><topic>p18</topic><topic>Pharmacology. Drug treatments</topic><topic>Protein Kinase Inhibitors</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Suppressor Proteins</topic><topic>Tumors of the nervous system. Phacomatoses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Diccianni, Mitchell B.</creatorcontrib><creatorcontrib>Chau, Lan S.</creatorcontrib><creatorcontrib>Batova, Ayse</creatorcontrib><creatorcontrib>Vu, Thai Q.</creatorcontrib><creatorcontrib>Yu, Alice L.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Diccianni, Mitchell B.</au><au>Chau, Lan S.</au><au>Batova, Ayse</au><au>Vu, Thai Q.</au><au>Yu, Alice L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The p16 and p18 tumor suppressor genes in neuroblastoma: implications for drug resistance</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>1996-07-12</date><risdate>1996</risdate><volume>104</volume><issue>2</issue><spage>183</spage><epage>192</epage><pages>183-192</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><coden>CALEDQ</coden><abstract>The cyclin dependent kinase inhibitors p16 and p18 were investigated in neuroblastoma. Only one of 19 neuroblastoma cell lines, an adriamycin-resistant variant, and none of 5 primary neuroblastoma, was deleted for p16 while its parental drug sensitive cell line is p16 intact. The region of deletion minimally extended centromeric to include p15, and telomeric to interferon-β. This is the first report of a p16 gene alteration in neuroblastoma. No p16 gene hypermethylation or mutations were found. No homozygous deletions of p18 in these samples were found, although several instances of loss of heterozygosity are suspected. No p18 point mutations were detected. We conclude that (1) neither p16 nor p18 are likely involved in the pathogenesis of neuroblastoma; and (2) the role of p16, or another 9p21 gene, in the development of drug resistance warrants further investigation.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>8665486</pmid><doi>10.1016/0304-3835(96)04250-4</doi><tpages>10</tpages></addata></record> |
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| ispartof | Cancer letters, 1996-07, Vol.104 (2), p.183-192 |
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| language | eng |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Antineoplastic agents Base Sequence Biological and medical sciences Carrier Proteins - genetics Cell Cycle Proteins Chemotherapy Chromosome Deletion Chromosome Mapping Chromosomes, Human, Pair 9 Cyclin-dependent kinase inhibitor Cyclin-Dependent Kinase Inhibitor p16 Cyclin-Dependent Kinase Inhibitor p18 Enzyme Inhibitors Genes, Tumor Suppressor Humans Hypermethylation Medical sciences Molecular Sequence Data Neuroblastoma Neuroblastoma - genetics Neurology p16 p18 Pharmacology. Drug treatments Protein Kinase Inhibitors Tumor Cells, Cultured Tumor Suppressor Proteins Tumors of the nervous system. Phacomatoses |
| title | The p16 and p18 tumor suppressor genes in neuroblastoma: implications for drug resistance |
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