Genetic changes in familial prostate cancer by comparative genomic hybridization
Background Germline mutations in recessive cancer predisposition genes are uncovered by somatic genetic deletions during tumor development. Analysis of genetic changes in tumor tissues from patients with an inherited predisposition may therefore highlight regions of the genome containing susceptibil...
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| Veröffentlicht in: | The Prostate 2001-02, Vol.46 (3), p.233-239 |
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| creator | Rökman, Annika Koivisto, Pasi A. Matikainen, Mika P. Kuukasjärvi, Tuula Poutiainen, Marita Helin, Heikki J. Karhu, Ritva Kallioniemi, Olli-P. Schleutker, Johanna |
| description | Background
Germline mutations in recessive cancer predisposition genes are uncovered by somatic genetic deletions during tumor development. Analysis of genetic changes in tumor tissues from patients with an inherited predisposition may therefore highlight regions of the genome containing susceptibility or modifier genes. Our aim was to characterize genetic changes in familial prostate cancer
Methods
Twenty‐one primary prostate cancers from 19 Finnish prostate cancer families were analyzed for somatic genetic changes by comparative genomic hybridization (CGH).
Results
The average number of genetic alterations per tumor was 4.0 ± 1.9, distributed equally among losses and gains. The most common losses were found at chromosomal regions 13q14–q22 (29%), 8p12‐pter (24%), and 6q13–q16 (14%), and the most common gains at 19p (25%), 19q (14%) and 7q (14%).
Conclusions
These results suggest that prostate cancers in genetically predisposed individuals arise for the most part through similar somatic genetic progression pathways as sporadic prostate cancers. This also implies that the biological properties of tumors from the two groups may not be different from one another. Prostate 46:233–239, 2001. © 2001 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/1097-0045(20010215)46:3<233::AID-PROS1028>3.0.CO;2-W |
| format | Article |
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Germline mutations in recessive cancer predisposition genes are uncovered by somatic genetic deletions during tumor development. Analysis of genetic changes in tumor tissues from patients with an inherited predisposition may therefore highlight regions of the genome containing susceptibility or modifier genes. Our aim was to characterize genetic changes in familial prostate cancer
Methods
Twenty‐one primary prostate cancers from 19 Finnish prostate cancer families were analyzed for somatic genetic changes by comparative genomic hybridization (CGH).
Results
The average number of genetic alterations per tumor was 4.0 ± 1.9, distributed equally among losses and gains. The most common losses were found at chromosomal regions 13q14–q22 (29%), 8p12‐pter (24%), and 6q13–q16 (14%), and the most common gains at 19p (25%), 19q (14%) and 7q (14%).
Conclusions
These results suggest that prostate cancers in genetically predisposed individuals arise for the most part through similar somatic genetic progression pathways as sporadic prostate cancers. This also implies that the biological properties of tumors from the two groups may not be different from one another. Prostate 46:233–239, 2001. © 2001 Wiley‐Liss, Inc.</description><identifier>ISSN: 0270-4137</identifier><identifier>EISSN: 1097-0045</identifier><identifier>DOI: 10.1002/1097-0045(20010215)46:3<233::AID-PROS1028>3.0.CO;2-W</identifier><identifier>PMID: 11170152</identifier><identifier>CODEN: PRSTDS</identifier><language>eng</language><publisher>New York: John Wiley & Sons, Inc</publisher><subject>Aged ; Aged, 80 and over ; Biological and medical sciences ; cancer predisposition ; Carcinoma - genetics ; Chromosome Aberrations ; deletion ; Genetic Predisposition to Disease - genetics ; hereditary prostate cancer ; Humans ; Karyotyping ; Male ; Medical sciences ; Middle Aged ; molecular cytogenetics ; Nephrology. Urinary tract diseases ; Nucleic Acid Hybridization ; Prostatic Neoplasms - genetics ; Tumors of the urinary system ; Urinary tract. Prostate gland</subject><ispartof>The Prostate, 2001-02, Vol.46 (3), p.233-239</ispartof><rights>Copyright © 2001 Wiley‐Liss, Inc.</rights><rights>2001 INIST-CNRS</rights><rights>Copyright 2001 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4328-1251363312a3a33265846897ffa664b716b11725d37740dbfb292b4684591aab3</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%2F1097-0045%2820010215%2946%3A3%3C233%3A%3AAID-PROS1028%3E3.0.CO%3B2-W$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2F1097-0045%2820010215%2946%3A3%3C233%3A%3AAID-PROS1028%3E3.0.CO%3B2-W$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=877206$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11170152$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rökman, Annika</creatorcontrib><creatorcontrib>Koivisto, Pasi A.</creatorcontrib><creatorcontrib>Matikainen, Mika P.</creatorcontrib><creatorcontrib>Kuukasjärvi, Tuula</creatorcontrib><creatorcontrib>Poutiainen, Marita</creatorcontrib><creatorcontrib>Helin, Heikki J.</creatorcontrib><creatorcontrib>Karhu, Ritva</creatorcontrib><creatorcontrib>Kallioniemi, Olli-P.</creatorcontrib><creatorcontrib>Schleutker, Johanna</creatorcontrib><title>Genetic changes in familial prostate cancer by comparative genomic hybridization</title><title>The Prostate</title><addtitle>Prostate</addtitle><description>Background
Germline mutations in recessive cancer predisposition genes are uncovered by somatic genetic deletions during tumor development. Analysis of genetic changes in tumor tissues from patients with an inherited predisposition may therefore highlight regions of the genome containing susceptibility or modifier genes. Our aim was to characterize genetic changes in familial prostate cancer
Methods
Twenty‐one primary prostate cancers from 19 Finnish prostate cancer families were analyzed for somatic genetic changes by comparative genomic hybridization (CGH).
Results
The average number of genetic alterations per tumor was 4.0 ± 1.9, distributed equally among losses and gains. The most common losses were found at chromosomal regions 13q14–q22 (29%), 8p12‐pter (24%), and 6q13–q16 (14%), and the most common gains at 19p (25%), 19q (14%) and 7q (14%).
Conclusions
These results suggest that prostate cancers in genetically predisposed individuals arise for the most part through similar somatic genetic progression pathways as sporadic prostate cancers. This also implies that the biological properties of tumors from the two groups may not be different from one another. Prostate 46:233–239, 2001. © 2001 Wiley‐Liss, Inc.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>cancer predisposition</subject><subject>Carcinoma - genetics</subject><subject>Chromosome Aberrations</subject><subject>deletion</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>hereditary prostate cancer</subject><subject>Humans</subject><subject>Karyotyping</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>molecular cytogenetics</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nucleic Acid Hybridization</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. Prostate gland</subject><issn>0270-4137</issn><issn>1097-0045</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkM1uEzEYRS0EoiHwCmgkJFQWE_w39kyokKoAoaiQihQi2Hz6PPG0pvMT7AkQnh5HScOKBStLV9fH14eQE0ZHjFL-nNFCp5TK7JhTyihn2TOpxuKECzEen569Si8-zuYxz1-KER1NZi94urhDBodrd8mAck1TyYQ-Ig9C-LbFRPJ9csQY05RlfEAupra1vSuT8hrbKxsS1yYVNq52WCcr34Uee5uU2JbWJ2aTlF2zQo-9-2GTK9t2Tbx6vTHeLd3vmHbtQ3KvwjrYR_tzSD69eX05eZuez6Znk9PztJSC5ynjGRNKCMZRoBBcZblUeaGrCpWSRjNl4kaeLYXWki5NZXjBTazIrGCIRgzJ0x03jvy-tqGHxoXS1jW2tlsH0FQJzlURi5e7Yhl_E7ytYOVdg34DjMLWNGyVwVYZ3JoGqUBANA0QTcOt6ZhRmMyAwyJiH-_fX5vGLv9C92pj4cm-gKHEuvLRoQuHXq41jxOH5Muu9dPVdvNf0_6x7JBFdrpju9DbXwc2-htQWugMFh-mULz_St_N5ww-iz8ZzLKq</recordid><startdate>20010215</startdate><enddate>20010215</enddate><creator>Rökman, Annika</creator><creator>Koivisto, Pasi A.</creator><creator>Matikainen, Mika P.</creator><creator>Kuukasjärvi, Tuula</creator><creator>Poutiainen, Marita</creator><creator>Helin, Heikki J.</creator><creator>Karhu, Ritva</creator><creator>Kallioniemi, Olli-P.</creator><creator>Schleutker, Johanna</creator><general>John Wiley & Sons, Inc</general><general>Wiley-Liss</general><scope>BSCLL</scope><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>20010215</creationdate><title>Genetic changes in familial prostate cancer by comparative genomic hybridization</title><author>Rökman, Annika ; Koivisto, Pasi A. ; Matikainen, Mika P. ; Kuukasjärvi, Tuula ; Poutiainen, Marita ; Helin, Heikki J. ; Karhu, Ritva ; Kallioniemi, Olli-P. ; Schleutker, Johanna</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4328-1251363312a3a33265846897ffa664b716b11725d37740dbfb292b4684591aab3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biological and medical sciences</topic><topic>cancer predisposition</topic><topic>Carcinoma - genetics</topic><topic>Chromosome Aberrations</topic><topic>deletion</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>hereditary prostate cancer</topic><topic>Humans</topic><topic>Karyotyping</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>molecular cytogenetics</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nucleic Acid Hybridization</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rökman, Annika</creatorcontrib><creatorcontrib>Koivisto, Pasi A.</creatorcontrib><creatorcontrib>Matikainen, Mika P.</creatorcontrib><creatorcontrib>Kuukasjärvi, Tuula</creatorcontrib><creatorcontrib>Poutiainen, Marita</creatorcontrib><creatorcontrib>Helin, Heikki J.</creatorcontrib><creatorcontrib>Karhu, Ritva</creatorcontrib><creatorcontrib>Kallioniemi, Olli-P.</creatorcontrib><creatorcontrib>Schleutker, Johanna</creatorcontrib><collection>Istex</collection><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>The Prostate</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rökman, Annika</au><au>Koivisto, Pasi A.</au><au>Matikainen, Mika P.</au><au>Kuukasjärvi, Tuula</au><au>Poutiainen, Marita</au><au>Helin, Heikki J.</au><au>Karhu, Ritva</au><au>Kallioniemi, Olli-P.</au><au>Schleutker, Johanna</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic changes in familial prostate cancer by comparative genomic hybridization</atitle><jtitle>The Prostate</jtitle><addtitle>Prostate</addtitle><date>2001-02-15</date><risdate>2001</risdate><volume>46</volume><issue>3</issue><spage>233</spage><epage>239</epage><pages>233-239</pages><issn>0270-4137</issn><eissn>1097-0045</eissn><coden>PRSTDS</coden><abstract>Background
Germline mutations in recessive cancer predisposition genes are uncovered by somatic genetic deletions during tumor development. Analysis of genetic changes in tumor tissues from patients with an inherited predisposition may therefore highlight regions of the genome containing susceptibility or modifier genes. Our aim was to characterize genetic changes in familial prostate cancer
Methods
Twenty‐one primary prostate cancers from 19 Finnish prostate cancer families were analyzed for somatic genetic changes by comparative genomic hybridization (CGH).
Results
The average number of genetic alterations per tumor was 4.0 ± 1.9, distributed equally among losses and gains. The most common losses were found at chromosomal regions 13q14–q22 (29%), 8p12‐pter (24%), and 6q13–q16 (14%), and the most common gains at 19p (25%), 19q (14%) and 7q (14%).
Conclusions
These results suggest that prostate cancers in genetically predisposed individuals arise for the most part through similar somatic genetic progression pathways as sporadic prostate cancers. This also implies that the biological properties of tumors from the two groups may not be different from one another. Prostate 46:233–239, 2001. © 2001 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>John Wiley & Sons, Inc</pub><pmid>11170152</pmid><doi>10.1002/1097-0045(20010215)46:3<233::AID-PROS1028>3.0.CO;2-W</doi><tpages>7</tpages></addata></record> |
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| ispartof | The Prostate, 2001-02, Vol.46 (3), p.233-239 |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Aged Aged, 80 and over Biological and medical sciences cancer predisposition Carcinoma - genetics Chromosome Aberrations deletion Genetic Predisposition to Disease - genetics hereditary prostate cancer Humans Karyotyping Male Medical sciences Middle Aged molecular cytogenetics Nephrology. Urinary tract diseases Nucleic Acid Hybridization Prostatic Neoplasms - genetics Tumors of the urinary system Urinary tract. Prostate gland |
| title | Genetic changes in familial prostate cancer by comparative genomic hybridization |
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