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Copy number variations of chromosome 17p13.1 might be linked to high risk of lung cancer in heavy smokers
Lung cancer is the most common cause of cancer death worldwide. Smoking is known as the strongest single factor in the development of lung cancer. However, there are inherited genetic factors that cause different responses to cigarette smoking exposure among individuals. We tried to identify these d...
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| Published in: | Molecular biology reports 2011-11, Vol.38 (8), p.5211-5217 |
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| cites | cdi_FETCH-LOGICAL-c403t-898c47ef37abeb32efe7ca5600b3ddfd59808b66e8d290dd9b13dd00dd64ba93 |
| container_end_page | 5217 |
| container_issue | 8 |
| container_start_page | 5211 |
| container_title | Molecular biology reports |
| container_volume | 38 |
| creator | Lee, Minhyeok Lee, Yeiwon Cho, Hyun-Jung Hong, Jeeyoung Kwon, Sun-Jung Park, Chang-Gyo Lee, Hoi-Young Son, Ji-Woong Kang, Jaeku |
| description | Lung cancer is the most common cause of cancer death worldwide. Smoking is known as the strongest single factor in the development of lung cancer. However, there are inherited genetic factors that cause different responses to cigarette smoking exposure among individuals. We tried to identify these differences in heavy smokers by examining copy number variations (CNVs) between lung cancer patients and healthy controls. Analysis by array comparative genomic hybridization which was tested with 20-person training set (10 lung cancer patients, 10 healthy controls) showed 26 significant (adjusted
P
|
| doi_str_mv | 10.1007/s11033-010-0672-3 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_900623007</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>900623007</sourcerecordid><originalsourceid>FETCH-LOGICAL-c403t-898c47ef37abeb32efe7ca5600b3ddfd59808b66e8d290dd9b13dd00dd64ba93</originalsourceid><addsrcrecordid>eNp9kU-P0zAQxS0EYsvCB-CCLC5wyTITO7FzRBX_pJW47N2yk0nrbWIXO1mp3x5XXUBCgpOt8e-98cxj7DXCDQKoDxkRhKgAoYJW1ZV4wjbYKFHJTumnbAMCsJK6wSv2Iud7AJComufsqsYahG5gw_w2Hk88rLOjxB9s8nbxMWQeR97vU5xjjjNxVEcUN8hnv9sv3BGffDjQwJfI96XEk8-Hs2Raw473NvTFzAe-J_tw4nmOB0r5JXs22inTq8fzmt19_nS3_Vrdfv_ybfvxtuoliKXSne6lolEo68iJmkZSvW1aACeGYRyaToN2bUt6qDsYhs5hqUO5tdLZTlyzdxfbY4o_VsqLmX3uaZpsoLhm0wG0tSjbK-T7_5IIqLpGQS0L-vYv9D6uKZQxTPmvllK3TYHwAvUp5pxoNMfkZ5tOxcmc8zKXvEzJy5zzMqJo3jwar26m4bfiV0AFqC9ALk9hR-lP53-7_gRby58x</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>898844865</pqid></control><display><type>article</type><title>Copy number variations of chromosome 17p13.1 might be linked to high risk of lung cancer in heavy smokers</title><source>Springer Nature</source><creator>Lee, Minhyeok ; Lee, Yeiwon ; Cho, Hyun-Jung ; Hong, Jeeyoung ; Kwon, Sun-Jung ; Park, Chang-Gyo ; Lee, Hoi-Young ; Son, Ji-Woong ; Kang, Jaeku</creator><creatorcontrib>Lee, Minhyeok ; Lee, Yeiwon ; Cho, Hyun-Jung ; Hong, Jeeyoung ; Kwon, Sun-Jung ; Park, Chang-Gyo ; Lee, Hoi-Young ; Son, Ji-Woong ; Kang, Jaeku</creatorcontrib><description>Lung cancer is the most common cause of cancer death worldwide. Smoking is known as the strongest single factor in the development of lung cancer. However, there are inherited genetic factors that cause different responses to cigarette smoking exposure among individuals. We tried to identify these differences in heavy smokers by examining copy number variations (CNVs) between lung cancer patients and healthy controls. Analysis by array comparative genomic hybridization which was tested with 20-person training set (10 lung cancer patients, 10 healthy controls) showed 26 significant (adjusted
P
< 0.05) clones with either copy number gains or losses. Three genes,
KCTD11
,
FGF11
, and
PTPRH
on chromosomal regions 17p13.1 (
KCTD11
and
FGF11
) and 19q13.42 (
PTPRH
), were selected (adjusted
P
< 0.001) and tested by real-time quantitative PCR with 34 healthy controls and 54 lung cancer patients.
KCTD11
on the chromosomal region 17p13.1 showed significant high odds ratio (OR = 16.0) in heavy smokers, implying that this is a susceptibility region for lung cancer in this group. Therefore, CNVs of 17p13.1 is a promising candidate to identify individuals with a high genetic risk for the development of lung cancer.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-010-0672-3</identifier><identifier>PMID: 21203850</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Animal Anatomy ; Animal Biochemistry ; Biomedical and Life Sciences ; Case-Control Studies ; Cell Line, Tumor ; chromosome 17 ; Chromosomes ; Chromosomes, Human, Pair 17 - genetics ; Cigarette smoking ; Cluster Analysis ; Comparative Genomic Hybridization ; copy number ; DNA Copy Number Variations - genetics ; Gene Expression Regulation, Neoplastic ; Gene Frequency - genetics ; Genetic factors ; Genetic Predisposition to Disease ; genomics ; Histology ; Humans ; Life Sciences ; Lung cancer ; Lung Neoplasms - genetics ; Molecular biology ; Morphology ; Odds Ratio ; Polymerase chain reaction ; Real-Time Polymerase Chain Reaction ; Risk Factors ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Smoking ; Smoking - genetics</subject><ispartof>Molecular biology reports, 2011-11, Vol.38 (8), p.5211-5217</ispartof><rights>Springer Science+Business Media B.V. 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c403t-898c47ef37abeb32efe7ca5600b3ddfd59808b66e8d290dd9b13dd00dd64ba93</citedby><cites>FETCH-LOGICAL-c403t-898c47ef37abeb32efe7ca5600b3ddfd59808b66e8d290dd9b13dd00dd64ba93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21203850$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Minhyeok</creatorcontrib><creatorcontrib>Lee, Yeiwon</creatorcontrib><creatorcontrib>Cho, Hyun-Jung</creatorcontrib><creatorcontrib>Hong, Jeeyoung</creatorcontrib><creatorcontrib>Kwon, Sun-Jung</creatorcontrib><creatorcontrib>Park, Chang-Gyo</creatorcontrib><creatorcontrib>Lee, Hoi-Young</creatorcontrib><creatorcontrib>Son, Ji-Woong</creatorcontrib><creatorcontrib>Kang, Jaeku</creatorcontrib><title>Copy number variations of chromosome 17p13.1 might be linked to high risk of lung cancer in heavy smokers</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>Lung cancer is the most common cause of cancer death worldwide. Smoking is known as the strongest single factor in the development of lung cancer. However, there are inherited genetic factors that cause different responses to cigarette smoking exposure among individuals. We tried to identify these differences in heavy smokers by examining copy number variations (CNVs) between lung cancer patients and healthy controls. Analysis by array comparative genomic hybridization which was tested with 20-person training set (10 lung cancer patients, 10 healthy controls) showed 26 significant (adjusted
P
< 0.05) clones with either copy number gains or losses. Three genes,
KCTD11
,
FGF11
, and
PTPRH
on chromosomal regions 17p13.1 (
KCTD11
and
FGF11
) and 19q13.42 (
PTPRH
), were selected (adjusted
P
< 0.001) and tested by real-time quantitative PCR with 34 healthy controls and 54 lung cancer patients.
KCTD11
on the chromosomal region 17p13.1 showed significant high odds ratio (OR = 16.0) in heavy smokers, implying that this is a susceptibility region for lung cancer in this group. Therefore, CNVs of 17p13.1 is a promising candidate to identify individuals with a high genetic risk for the development of lung cancer.</description><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Case-Control Studies</subject><subject>Cell Line, Tumor</subject><subject>chromosome 17</subject><subject>Chromosomes</subject><subject>Chromosomes, Human, Pair 17 - genetics</subject><subject>Cigarette smoking</subject><subject>Cluster Analysis</subject><subject>Comparative Genomic Hybridization</subject><subject>copy number</subject><subject>DNA Copy Number Variations - genetics</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Frequency - genetics</subject><subject>Genetic factors</subject><subject>Genetic Predisposition to Disease</subject><subject>genomics</subject><subject>Histology</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - genetics</subject><subject>Molecular biology</subject><subject>Morphology</subject><subject>Odds Ratio</subject><subject>Polymerase chain reaction</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Risk Factors</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Smoking</subject><subject>Smoking - genetics</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNp9kU-P0zAQxS0EYsvCB-CCLC5wyTITO7FzRBX_pJW47N2yk0nrbWIXO1mp3x5XXUBCgpOt8e-98cxj7DXCDQKoDxkRhKgAoYJW1ZV4wjbYKFHJTumnbAMCsJK6wSv2Iud7AJComufsqsYahG5gw_w2Hk88rLOjxB9s8nbxMWQeR97vU5xjjjNxVEcUN8hnv9sv3BGffDjQwJfI96XEk8-Hs2Raw473NvTFzAe-J_tw4nmOB0r5JXs22inTq8fzmt19_nS3_Vrdfv_ybfvxtuoliKXSne6lolEo68iJmkZSvW1aACeGYRyaToN2bUt6qDsYhs5hqUO5tdLZTlyzdxfbY4o_VsqLmX3uaZpsoLhm0wG0tSjbK-T7_5IIqLpGQS0L-vYv9D6uKZQxTPmvllK3TYHwAvUp5pxoNMfkZ5tOxcmc8zKXvEzJy5zzMqJo3jwar26m4bfiV0AFqC9ALk9hR-lP53-7_gRby58x</recordid><startdate>20111101</startdate><enddate>20111101</enddate><creator>Lee, Minhyeok</creator><creator>Lee, Yeiwon</creator><creator>Cho, Hyun-Jung</creator><creator>Hong, Jeeyoung</creator><creator>Kwon, Sun-Jung</creator><creator>Park, Chang-Gyo</creator><creator>Lee, Hoi-Young</creator><creator>Son, Ji-Woong</creator><creator>Kang, Jaeku</creator><general>Springer Netherlands</general><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>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7U7</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>20111101</creationdate><title>Copy number variations of chromosome 17p13.1 might be linked to high risk of lung cancer in heavy smokers</title><author>Lee, Minhyeok ; Lee, Yeiwon ; Cho, Hyun-Jung ; Hong, Jeeyoung ; Kwon, Sun-Jung ; Park, Chang-Gyo ; Lee, Hoi-Young ; Son, Ji-Woong ; Kang, Jaeku</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c403t-898c47ef37abeb32efe7ca5600b3ddfd59808b66e8d290dd9b13dd00dd64ba93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Case-Control Studies</topic><topic>Cell Line, Tumor</topic><topic>chromosome 17</topic><topic>Chromosomes</topic><topic>Chromosomes, Human, Pair 17 - genetics</topic><topic>Cigarette smoking</topic><topic>Cluster Analysis</topic><topic>Comparative Genomic Hybridization</topic><topic>copy number</topic><topic>DNA Copy Number Variations - genetics</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Frequency - genetics</topic><topic>Genetic factors</topic><topic>Genetic Predisposition to Disease</topic><topic>genomics</topic><topic>Histology</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - genetics</topic><topic>Molecular biology</topic><topic>Morphology</topic><topic>Odds Ratio</topic><topic>Polymerase chain reaction</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Risk Factors</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Smoking</topic><topic>Smoking - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Minhyeok</creatorcontrib><creatorcontrib>Lee, Yeiwon</creatorcontrib><creatorcontrib>Cho, Hyun-Jung</creatorcontrib><creatorcontrib>Hong, Jeeyoung</creatorcontrib><creatorcontrib>Kwon, Sun-Jung</creatorcontrib><creatorcontrib>Park, Chang-Gyo</creatorcontrib><creatorcontrib>Lee, Hoi-Young</creatorcontrib><creatorcontrib>Son, Ji-Woong</creatorcontrib><creatorcontrib>Kang, Jaeku</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>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Science Database (ProQuest)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Minhyeok</au><au>Lee, Yeiwon</au><au>Cho, Hyun-Jung</au><au>Hong, Jeeyoung</au><au>Kwon, Sun-Jung</au><au>Park, Chang-Gyo</au><au>Lee, Hoi-Young</au><au>Son, Ji-Woong</au><au>Kang, Jaeku</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Copy number variations of chromosome 17p13.1 might be linked to high risk of lung cancer in heavy smokers</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2011-11-01</date><risdate>2011</risdate><volume>38</volume><issue>8</issue><spage>5211</spage><epage>5217</epage><pages>5211-5217</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>Lung cancer is the most common cause of cancer death worldwide. Smoking is known as the strongest single factor in the development of lung cancer. However, there are inherited genetic factors that cause different responses to cigarette smoking exposure among individuals. We tried to identify these differences in heavy smokers by examining copy number variations (CNVs) between lung cancer patients and healthy controls. Analysis by array comparative genomic hybridization which was tested with 20-person training set (10 lung cancer patients, 10 healthy controls) showed 26 significant (adjusted
P
< 0.05) clones with either copy number gains or losses. Three genes,
KCTD11
,
FGF11
, and
PTPRH
on chromosomal regions 17p13.1 (
KCTD11
and
FGF11
) and 19q13.42 (
PTPRH
), were selected (adjusted
P
< 0.001) and tested by real-time quantitative PCR with 34 healthy controls and 54 lung cancer patients.
KCTD11
on the chromosomal region 17p13.1 showed significant high odds ratio (OR = 16.0) in heavy smokers, implying that this is a susceptibility region for lung cancer in this group. Therefore, CNVs of 17p13.1 is a promising candidate to identify individuals with a high genetic risk for the development of lung cancer.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>21203850</pmid><doi>10.1007/s11033-010-0672-3</doi><tpages>7</tpages></addata></record> |
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| ispartof | Molecular biology reports, 2011-11, Vol.38 (8), p.5211-5217 |
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| language | eng |
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| source | Springer Nature |
| subjects | Animal Anatomy Animal Biochemistry Biomedical and Life Sciences Case-Control Studies Cell Line, Tumor chromosome 17 Chromosomes Chromosomes, Human, Pair 17 - genetics Cigarette smoking Cluster Analysis Comparative Genomic Hybridization copy number DNA Copy Number Variations - genetics Gene Expression Regulation, Neoplastic Gene Frequency - genetics Genetic factors Genetic Predisposition to Disease genomics Histology Humans Life Sciences Lung cancer Lung Neoplasms - genetics Molecular biology Morphology Odds Ratio Polymerase chain reaction Real-Time Polymerase Chain Reaction Risk Factors RNA, Messenger - genetics RNA, Messenger - metabolism Smoking Smoking - genetics |
| title | Copy number variations of chromosome 17p13.1 might be linked to high risk of lung cancer in heavy smokers |
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