Loss of the Association between Telomere Length and Mitochondrial DNA Copy Number Contribute to Colorectal Carcinogenesis
Positive association between telomere length and mitochondrial DNA (mtDNA) copy number were introduced in healthy and patients with psychiatric disorder. Based on frequent genetic changes of telomere and mitochondria in colorectal carcinomas (CRC), we studied their clinical characteristics and their...
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Veröffentlicht in: | Pathology oncology research 2018-04, Vol.24 (2), p.323-328 |
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description | Positive association between telomere length and mitochondrial DNA (mtDNA) copy number were introduced in healthy and patients with psychiatric disorder. Based on frequent genetic changes of telomere and mitochondria in colorectal carcinomas (CRC), we studied their clinical characteristics and their association in colorectal carcinogenesis. DNA was extracted from 109 CRCs, 64 colorectal tubular adenomas (TAs), and 28 serrated polyps (SPs), and then, telomere length and mtDNA copy number were analyzed in these legions by using a real-time PCR assay. Telomere length and mtDNA copy number (mean ± S.D) in CRCs was 1.87 ± 1.52 and 1.61 ± 1.37, respectively. In TAs and SPs, relative mtDNA copy number was 0.92 ± 0.71 and 1.84 ± 1.06, respectively, shoing statistical difference (
p
= 0.017). However, telomere length was similar in these precancerous legions. Telomere length and mtDNA copy number did not show clinical and prognostic values in CRCs, however, positive correlation between telomere length and mitochondrial DNA copy number were found in CRC (
r
= 0.408,
p
|
doi_str_mv | 10.1007/s12253-017-0245-z |
format | Article |
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p
= 0.017). However, telomere length was similar in these precancerous legions. Telomere length and mtDNA copy number did not show clinical and prognostic values in CRCs, however, positive correlation between telomere length and mitochondrial DNA copy number were found in CRC (
r
= 0.408,
p
< 0.001). However, this association was not shown in precancerous lesions (
r
= −0.031,
p
= 0.765). This result suggests that loss of co-regulation between telomeres and mitochondrial function may induce the initiation or play a role as trigger factor of colorectal carcinogenesis.</description><identifier>ISSN: 1219-4956</identifier><identifier>EISSN: 1532-2807</identifier><identifier>DOI: 10.1007/s12253-017-0245-z</identifier><identifier>PMID: 28488129</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Carcinogenesis ; Chromosomes ; Colorectal cancer ; Colorectal carcinoma ; Copy number ; Genetic recombination ; Immunology ; Lesions ; Mitochondrial DNA ; Oncology ; Original Article ; Pathology ; Polyps ; Telomeres ; Trigger factor ; Yeast</subject><ispartof>Pathology oncology research, 2018-04, Vol.24 (2), p.323-328</ispartof><rights>Arányi Lajos Foundation 2017</rights><rights>Pathology & Oncology Research is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-c34522d8e2c01a9bfe9f24b41a83ce146773d1219f0a2d8c8dbafdcc1dd943ad3</citedby><cites>FETCH-LOGICAL-c372t-c34522d8e2c01a9bfe9f24b41a83ce146773d1219f0a2d8c8dbafdcc1dd943ad3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12253-017-0245-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12253-017-0245-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28488129$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Hyunsu</creatorcontrib><creatorcontrib>Cho, Ji-Hyoung</creatorcontrib><creatorcontrib>Park, Won-Jin</creatorcontrib><creatorcontrib>Jung, Soo-Jung</creatorcontrib><creatorcontrib>Choi, In-Jang</creatorcontrib><creatorcontrib>Lee, Jae-Ho</creatorcontrib><title>Loss of the Association between Telomere Length and Mitochondrial DNA Copy Number Contribute to Colorectal Carcinogenesis</title><title>Pathology oncology research</title><addtitle>Pathol. Oncol. Res</addtitle><addtitle>Pathol Oncol Res</addtitle><description>Positive association between telomere length and mitochondrial DNA (mtDNA) copy number were introduced in healthy and patients with psychiatric disorder. Based on frequent genetic changes of telomere and mitochondria in colorectal carcinomas (CRC), we studied their clinical characteristics and their association in colorectal carcinogenesis. DNA was extracted from 109 CRCs, 64 colorectal tubular adenomas (TAs), and 28 serrated polyps (SPs), and then, telomere length and mtDNA copy number were analyzed in these legions by using a real-time PCR assay. Telomere length and mtDNA copy number (mean ± S.D) in CRCs was 1.87 ± 1.52 and 1.61 ± 1.37, respectively. In TAs and SPs, relative mtDNA copy number was 0.92 ± 0.71 and 1.84 ± 1.06, respectively, shoing statistical difference (
p
= 0.017). However, telomere length was similar in these precancerous legions. Telomere length and mtDNA copy number did not show clinical and prognostic values in CRCs, however, positive correlation between telomere length and mitochondrial DNA copy number were found in CRC (
r
= 0.408,
p
< 0.001). However, this association was not shown in precancerous lesions (
r
= −0.031,
p
= 0.765). This result suggests that loss of co-regulation between telomeres and mitochondrial function may induce the initiation or play a role as trigger factor of colorectal carcinogenesis.</description><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Carcinogenesis</subject><subject>Chromosomes</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Copy number</subject><subject>Genetic recombination</subject><subject>Immunology</subject><subject>Lesions</subject><subject>Mitochondrial DNA</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Pathology</subject><subject>Polyps</subject><subject>Telomeres</subject><subject>Trigger factor</subject><subject>Yeast</subject><issn>1219-4956</issn><issn>1532-2807</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp1kMtOAjEUhhujEUQfwI1p4nq0l7kuCV4TxA2um057BoZAi20nBp7ekkFduWnPSb_zn_RD6JqSO0pIce8pYxlPCC0SwtIs2Z-gIc04S1hJitNYM1olaZXlA3Th_YrEmbzKz9GAlWlZUlYN0W5qvce2wWEJeOy9Va0MrTW4hvAFYPAc1nYDDvAUzCIssTQav7XBqqU12rVyjR9mYzyx2x2edZsaXKxNcG3dBcDBxm5tHagQwYl0qjV2AQZ86y_RWSPXHq6O9wh9PD3OJy_J9P35dTKeJooXLMQzzRjTJTBFqKzqBqqGpXVKZckV0DQvCq4PH22IjJgqdS0brRTVukq51HyEbvvcrbOfHfggVrZzJq4UjNAsywnnWaRoTykXhThoxNa1G-l2ghJxkC162SLKFgfZYh9nbo7JXb0B_TvxYzcCrAd8fDILcH-r_0_9BoMPjFg</recordid><startdate>20180401</startdate><enddate>20180401</enddate><creator>Lee, Hyunsu</creator><creator>Cho, Ji-Hyoung</creator><creator>Park, Won-Jin</creator><creator>Jung, Soo-Jung</creator><creator>Choi, In-Jang</creator><creator>Lee, Jae-Ho</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20180401</creationdate><title>Loss of the Association between Telomere Length and Mitochondrial DNA Copy Number Contribute to Colorectal Carcinogenesis</title><author>Lee, Hyunsu ; Cho, Ji-Hyoung ; Park, Won-Jin ; Jung, Soo-Jung ; Choi, In-Jang ; Lee, Jae-Ho</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-c34522d8e2c01a9bfe9f24b41a83ce146773d1219f0a2d8c8dbafdcc1dd943ad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Carcinogenesis</topic><topic>Chromosomes</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Copy number</topic><topic>Genetic recombination</topic><topic>Immunology</topic><topic>Lesions</topic><topic>Mitochondrial DNA</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Pathology</topic><topic>Polyps</topic><topic>Telomeres</topic><topic>Trigger factor</topic><topic>Yeast</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Hyunsu</creatorcontrib><creatorcontrib>Cho, Ji-Hyoung</creatorcontrib><creatorcontrib>Park, Won-Jin</creatorcontrib><creatorcontrib>Jung, Soo-Jung</creatorcontrib><creatorcontrib>Choi, In-Jang</creatorcontrib><creatorcontrib>Lee, Jae-Ho</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Nursing & Allied Health Premium</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><jtitle>Pathology oncology research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Hyunsu</au><au>Cho, Ji-Hyoung</au><au>Park, Won-Jin</au><au>Jung, Soo-Jung</au><au>Choi, In-Jang</au><au>Lee, Jae-Ho</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of the Association between Telomere Length and Mitochondrial DNA Copy Number Contribute to Colorectal Carcinogenesis</atitle><jtitle>Pathology oncology research</jtitle><stitle>Pathol. Oncol. Res</stitle><addtitle>Pathol Oncol Res</addtitle><date>2018-04-01</date><risdate>2018</risdate><volume>24</volume><issue>2</issue><spage>323</spage><epage>328</epage><pages>323-328</pages><issn>1219-4956</issn><eissn>1532-2807</eissn><abstract>Positive association between telomere length and mitochondrial DNA (mtDNA) copy number were introduced in healthy and patients with psychiatric disorder. Based on frequent genetic changes of telomere and mitochondria in colorectal carcinomas (CRC), we studied their clinical characteristics and their association in colorectal carcinogenesis. DNA was extracted from 109 CRCs, 64 colorectal tubular adenomas (TAs), and 28 serrated polyps (SPs), and then, telomere length and mtDNA copy number were analyzed in these legions by using a real-time PCR assay. Telomere length and mtDNA copy number (mean ± S.D) in CRCs was 1.87 ± 1.52 and 1.61 ± 1.37, respectively. In TAs and SPs, relative mtDNA copy number was 0.92 ± 0.71 and 1.84 ± 1.06, respectively, shoing statistical difference (
p
= 0.017). However, telomere length was similar in these precancerous legions. Telomere length and mtDNA copy number did not show clinical and prognostic values in CRCs, however, positive correlation between telomere length and mitochondrial DNA copy number were found in CRC (
r
= 0.408,
p
< 0.001). However, this association was not shown in precancerous lesions (
r
= −0.031,
p
= 0.765). This result suggests that loss of co-regulation between telomeres and mitochondrial function may induce the initiation or play a role as trigger factor of colorectal carcinogenesis.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>28488129</pmid><doi>10.1007/s12253-017-0245-z</doi><tpages>6</tpages></addata></record> |
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subjects | Biomedical and Life Sciences Biomedicine Cancer Research Carcinogenesis Chromosomes Colorectal cancer Colorectal carcinoma Copy number Genetic recombination Immunology Lesions Mitochondrial DNA Oncology Original Article Pathology Polyps Telomeres Trigger factor Yeast |
title | Loss of the Association between Telomere Length and Mitochondrial DNA Copy Number Contribute to Colorectal Carcinogenesis |
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