Chromosomal aberrations in sporadic pituitary tumors
Pituitary adenomas are common intracranial neoplasms that may be hormone‐secreting or nonfunctional. Genetic defects associated with some pituitary tumors have been identified, although our understanding of the underlying molecular mechanisms remains incomplete. We have studied 75 sporadic pituitary...
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| Veröffentlicht in: | International journal of cancer 2001-03, Vol.91 (6), p.809-814 |
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| creator | Trautmann, K. Thakker, R.V. Ellison, D.W. Ibrahim, A. Lees, P.D. Harding, B. Fischer, C. Popp, S. Bartram, C.R. Jauch, A. |
| description | Pituitary adenomas are common intracranial neoplasms that may be hormone‐secreting or nonfunctional. Genetic defects associated with some pituitary tumors have been identified, although our understanding of the underlying molecular mechanisms remains incomplete. We have studied 75 sporadic pituitary tumors, representing the major clinical subtypes, by comparative genomic hybridization (CGH) with the aim of assessing for DNA copy number changes. CGH revealed chromosomal imbalances in 34 adenomas (45.3%), whereby gains were 4.9 times more frequently observed than losses. Most of the genetic alterations detected by CGH affected entire chromosomes (108/131, 82.4%). Gain of genetic material was observed predominantly on chromosomes X (24/75, 32%), 19 (12/75, 16%), 12 (6/75, 6.7%), 7 and 9 (5/75, 6.7%), whereas loss of DNA sequences most frequently affected chromosomes 11 (4/75, 5.3%), 13 and 10 (3/75, 4%). There were no significant differences in the CGH results for the individual clinical subtypes of pituitary tumors. These results reveal a nonrandom pattern of chromosomal alterations in pituitary tumors, in particular gains of entire chromosomes, and this may contribute to the development of such neoplasms. © 2001 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/1097-0215(200102)9999:9999<::AID-IJC1127>3.0.CO;2-E |
| format | Article |
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Genetic defects associated with some pituitary tumors have been identified, although our understanding of the underlying molecular mechanisms remains incomplete. We have studied 75 sporadic pituitary tumors, representing the major clinical subtypes, by comparative genomic hybridization (CGH) with the aim of assessing for DNA copy number changes. CGH revealed chromosomal imbalances in 34 adenomas (45.3%), whereby gains were 4.9 times more frequently observed than losses. Most of the genetic alterations detected by CGH affected entire chromosomes (108/131, 82.4%). Gain of genetic material was observed predominantly on chromosomes X (24/75, 32%), 19 (12/75, 16%), 12 (6/75, 6.7%), 7 and 9 (5/75, 6.7%), whereas loss of DNA sequences most frequently affected chromosomes 11 (4/75, 5.3%), 13 and 10 (3/75, 4%). There were no significant differences in the CGH results for the individual clinical subtypes of pituitary tumors. These results reveal a nonrandom pattern of chromosomal alterations in pituitary tumors, in particular gains of entire chromosomes, and this may contribute to the development of such neoplasms. © 2001 Wiley‐Liss, Inc.</description><identifier>ISSN: 0020-7136</identifier><identifier>EISSN: 1097-0215</identifier><identifier>DOI: 10.1002/1097-0215(200102)9999:9999<::AID-IJC1127>3.0.CO;2-E</identifier><identifier>PMID: 11275984</identifier><identifier>CODEN: IJCNAW</identifier><language>eng</language><publisher>New York: John Wiley & Sons, Inc</publisher><subject>Adenoma - genetics ; Adenoma - metabolism ; Adult ; Aged ; Aged, 80 and over ; Biological and medical sciences ; Chromosome Aberrations ; chromosome X ; comparative genomic hybridization ; DNA, Neoplasm - analysis ; Endocrinopathies ; Female ; Gene Dosage ; Humans ; Hypothalamus. Hypophysis. Epiphysis (diseases) ; Immunoenzyme Techniques ; Karyotyping ; Male ; Medical sciences ; Middle Aged ; Neoplasm Proteins - metabolism ; Non tumoral diseases. Target tissue resistance. Benign neoplasms ; Nucleic Acid Hybridization ; Pituitary Neoplasms - genetics ; Pituitary Neoplasms - metabolism ; pituitary tumors ; X Chromosome - genetics</subject><ispartof>International journal of cancer, 2001-03, Vol.91 (6), p.809-814</ispartof><rights>Copyright © 2001 Wiley‐Liss, Inc.</rights><rights>2001 INIST-CNRS</rights><rights>Copyright 2001 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c5317-118b8126bf738b70b0ec94a193c015b001b201277e79bdfb4fade7d161ccc8163</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2F1097-0215%28200102%299999%3A9999%3C%3A%3AAID-IJC1127%3E3.0.CO%3B2-E$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2F1097-0215%28200102%299999%3A9999%3C%3A%3AAID-IJC1127%3E3.0.CO%3B2-E$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,782,786,1419,27931,27932,45581,45582</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=973601$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11275984$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Trautmann, K.</creatorcontrib><creatorcontrib>Thakker, R.V.</creatorcontrib><creatorcontrib>Ellison, D.W.</creatorcontrib><creatorcontrib>Ibrahim, A.</creatorcontrib><creatorcontrib>Lees, P.D.</creatorcontrib><creatorcontrib>Harding, B.</creatorcontrib><creatorcontrib>Fischer, C.</creatorcontrib><creatorcontrib>Popp, S.</creatorcontrib><creatorcontrib>Bartram, C.R.</creatorcontrib><creatorcontrib>Jauch, A.</creatorcontrib><title>Chromosomal aberrations in sporadic pituitary tumors</title><title>International journal of cancer</title><addtitle>Int J Cancer</addtitle><description>Pituitary adenomas are common intracranial neoplasms that may be hormone‐secreting or nonfunctional. Genetic defects associated with some pituitary tumors have been identified, although our understanding of the underlying molecular mechanisms remains incomplete. We have studied 75 sporadic pituitary tumors, representing the major clinical subtypes, by comparative genomic hybridization (CGH) with the aim of assessing for DNA copy number changes. CGH revealed chromosomal imbalances in 34 adenomas (45.3%), whereby gains were 4.9 times more frequently observed than losses. Most of the genetic alterations detected by CGH affected entire chromosomes (108/131, 82.4%). Gain of genetic material was observed predominantly on chromosomes X (24/75, 32%), 19 (12/75, 16%), 12 (6/75, 6.7%), 7 and 9 (5/75, 6.7%), whereas loss of DNA sequences most frequently affected chromosomes 11 (4/75, 5.3%), 13 and 10 (3/75, 4%). There were no significant differences in the CGH results for the individual clinical subtypes of pituitary tumors. These results reveal a nonrandom pattern of chromosomal alterations in pituitary tumors, in particular gains of entire chromosomes, and this may contribute to the development of such neoplasms. © 2001 Wiley‐Liss, Inc.</description><subject>Adenoma - genetics</subject><subject>Adenoma - metabolism</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>Chromosome Aberrations</subject><subject>chromosome X</subject><subject>comparative genomic hybridization</subject><subject>DNA, Neoplasm - analysis</subject><subject>Endocrinopathies</subject><subject>Female</subject><subject>Gene Dosage</subject><subject>Humans</subject><subject>Hypothalamus. Hypophysis. Epiphysis (diseases)</subject><subject>Immunoenzyme Techniques</subject><subject>Karyotyping</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Non tumoral diseases. Target tissue resistance. Benign neoplasms</subject><subject>Nucleic Acid Hybridization</subject><subject>Pituitary Neoplasms - genetics</subject><subject>Pituitary Neoplasms - metabolism</subject><subject>pituitary tumors</subject><subject>X Chromosome - genetics</subject><issn>0020-7136</issn><issn>1097-0215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkMFq3DAURUVoSaZpfyEYAqVdePqeZFv2pBSCO22nBGbRJlshyTJRsEcTyabk7ytjN910Uy2eQJx3dTmEXCGsEYB-QKh4ChTzdxQAgb6v4tlM4-Nmc737nO6-14iUf2JrWNf7K5puT8jqeesFWcUUSDmy4oy8CuEhpmAO2Sk5m9byqsxWJKvvvetdcL3sEqmM93Kw7hASe0jC0XnZWJ0c7TDaQfqnZBh758Nr8rKVXTBvlvuc3H7Z_qy_pTf7r7v6-ibVOUOeIpaqRFqolrNScVBgdJVJrJgGzFWsoyjEJtzwSjWtylrZGN5ggVrrEgt2Tt7OuUfvHkcTBtHboE3XyYNxYxCcA3DkE_hjBrV3IXjTiqO3fSwsEMQkU0xaxKRFzDLF5HEeQkSZYpEpmABR7wUV25h6sXw_qt40fzMXexG4XAAZtOxaLw_ahmeu4qwAjNTdTP2ynXn6n2b_7vXnif0GOxOZIQ</recordid><startdate>20010315</startdate><enddate>20010315</enddate><creator>Trautmann, K.</creator><creator>Thakker, R.V.</creator><creator>Ellison, D.W.</creator><creator>Ibrahim, A.</creator><creator>Lees, P.D.</creator><creator>Harding, B.</creator><creator>Fischer, C.</creator><creator>Popp, S.</creator><creator>Bartram, C.R.</creator><creator>Jauch, A.</creator><general>John Wiley & Sons, Inc</general><general>Wiley-Liss</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>20010315</creationdate><title>Chromosomal aberrations in sporadic pituitary tumors</title><author>Trautmann, K. ; Thakker, R.V. ; Ellison, D.W. ; Ibrahim, A. ; Lees, P.D. ; Harding, B. ; Fischer, C. ; Popp, S. ; Bartram, C.R. ; Jauch, A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5317-118b8126bf738b70b0ec94a193c015b001b201277e79bdfb4fade7d161ccc8163</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Adenoma - genetics</topic><topic>Adenoma - metabolism</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biological and medical sciences</topic><topic>Chromosome Aberrations</topic><topic>chromosome X</topic><topic>comparative genomic hybridization</topic><topic>DNA, Neoplasm - analysis</topic><topic>Endocrinopathies</topic><topic>Female</topic><topic>Gene Dosage</topic><topic>Humans</topic><topic>Hypothalamus. Hypophysis. Epiphysis (diseases)</topic><topic>Immunoenzyme Techniques</topic><topic>Karyotyping</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Non tumoral diseases. Target tissue resistance. Benign neoplasms</topic><topic>Nucleic Acid Hybridization</topic><topic>Pituitary Neoplasms - genetics</topic><topic>Pituitary Neoplasms - metabolism</topic><topic>pituitary tumors</topic><topic>X Chromosome - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Trautmann, K.</creatorcontrib><creatorcontrib>Thakker, R.V.</creatorcontrib><creatorcontrib>Ellison, D.W.</creatorcontrib><creatorcontrib>Ibrahim, A.</creatorcontrib><creatorcontrib>Lees, P.D.</creatorcontrib><creatorcontrib>Harding, B.</creatorcontrib><creatorcontrib>Fischer, C.</creatorcontrib><creatorcontrib>Popp, S.</creatorcontrib><creatorcontrib>Bartram, C.R.</creatorcontrib><creatorcontrib>Jauch, A.</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>International journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Trautmann, K.</au><au>Thakker, R.V.</au><au>Ellison, D.W.</au><au>Ibrahim, A.</au><au>Lees, P.D.</au><au>Harding, B.</au><au>Fischer, C.</au><au>Popp, S.</au><au>Bartram, C.R.</au><au>Jauch, A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chromosomal aberrations in sporadic pituitary tumors</atitle><jtitle>International journal of cancer</jtitle><addtitle>Int J Cancer</addtitle><date>2001-03-15</date><risdate>2001</risdate><volume>91</volume><issue>6</issue><spage>809</spage><epage>814</epage><pages>809-814</pages><issn>0020-7136</issn><eissn>1097-0215</eissn><coden>IJCNAW</coden><abstract>Pituitary adenomas are common intracranial neoplasms that may be hormone‐secreting or nonfunctional. Genetic defects associated with some pituitary tumors have been identified, although our understanding of the underlying molecular mechanisms remains incomplete. We have studied 75 sporadic pituitary tumors, representing the major clinical subtypes, by comparative genomic hybridization (CGH) with the aim of assessing for DNA copy number changes. CGH revealed chromosomal imbalances in 34 adenomas (45.3%), whereby gains were 4.9 times more frequently observed than losses. Most of the genetic alterations detected by CGH affected entire chromosomes (108/131, 82.4%). Gain of genetic material was observed predominantly on chromosomes X (24/75, 32%), 19 (12/75, 16%), 12 (6/75, 6.7%), 7 and 9 (5/75, 6.7%), whereas loss of DNA sequences most frequently affected chromosomes 11 (4/75, 5.3%), 13 and 10 (3/75, 4%). There were no significant differences in the CGH results for the individual clinical subtypes of pituitary tumors. These results reveal a nonrandom pattern of chromosomal alterations in pituitary tumors, in particular gains of entire chromosomes, and this may contribute to the development of such neoplasms. © 2001 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>John Wiley & Sons, Inc</pub><pmid>11275984</pmid><doi>10.1002/1097-0215(200102)9999:9999<::AID-IJC1127>3.0.CO;2-E</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenoma - genetics Adenoma - metabolism Adult Aged Aged, 80 and over Biological and medical sciences Chromosome Aberrations chromosome X comparative genomic hybridization DNA, Neoplasm - analysis Endocrinopathies Female Gene Dosage Humans Hypothalamus. Hypophysis. Epiphysis (diseases) Immunoenzyme Techniques Karyotyping Male Medical sciences Middle Aged Neoplasm Proteins - metabolism Non tumoral diseases. Target tissue resistance. Benign neoplasms Nucleic Acid Hybridization Pituitary Neoplasms - genetics Pituitary Neoplasms - metabolism pituitary tumors X Chromosome - genetics |
| title | Chromosomal aberrations in sporadic pituitary tumors |
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