Telomere shortening is associated with poor prognosis and telomerase activity correlates with DNA repair impairment in non-small cell lung cancer
Summary Background and purpose Telomere function and DNA damage response pathways are frequently inactivated in cancer. Moreover, some telomere-binding proteins have been implicated in DNA repair. The purpose of this work consists of evaluating the prognostic impact of telomere dysfunction and its r...
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| Veröffentlicht in: | Lung cancer (Amsterdam, Netherlands) Netherlands), 2008-06, Vol.60 (3), p.416-425 |
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| creator | Frías, Cristina García-Aranda, Cristina De Juan, Carmen Morán, Alberto Ortega, Paloma Gómez, Ana Hernando, Florentino López-Asenjo, Jose-Antonio Torres, Antonio-José Benito, Manuel Iniesta, Pilar |
| description | Summary Background and purpose Telomere function and DNA damage response pathways are frequently inactivated in cancer. Moreover, some telomere-binding proteins have been implicated in DNA repair. The purpose of this work consists of evaluating the prognostic impact of telomere dysfunction and its relationship with DNA repair systems in non-small cell lung cancer (NSCLC). Patients and methods We analysed 83 NSCLCs and their corresponding control samples obtained from patients submitted to surgery. Telomere function was evaluated by determining telomerase activity and telomere length. DNA repair expression assays were established by using cDNA arrays containing 96 DNA-repair genes and by Real Time Quantitative PCR. Results Our data indicated that telomere attrition was significantly associated with poor clinical outcome of patients ( P = 0.02), being this parameter a significant prognostic factor independent of tumour stage ( P = 0.012; relative risk = 1.887; 95% CI: 1.147–3.102). DNA-repair gene expression studies showed down regulation of DCLRE1C and GTF2H1 and a clear FLJ10858 up regulation in tumour tissues, as compared to controls. In addition, a number of genes related to DNA-repair were significantly down regulated in tumours that reactivated telomerase ( DCLRE1C , GTF2H1 , PARP-3 , MLH1 , and TRF2 ). Conclusions Telomere shortening emerged as a poor clinical evolution parameter in NSCLC. Moreover, results from this work suggest a relationship between the loss of several DNA repair genes and telomerase activity, which may be of relevance in the pathogenesis of non-small lung cancer. |
| doi_str_mv | 10.1016/j.lungcan.2007.11.001 |
| format | Article |
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Moreover, some telomere-binding proteins have been implicated in DNA repair. The purpose of this work consists of evaluating the prognostic impact of telomere dysfunction and its relationship with DNA repair systems in non-small cell lung cancer (NSCLC). Patients and methods We analysed 83 NSCLCs and their corresponding control samples obtained from patients submitted to surgery. Telomere function was evaluated by determining telomerase activity and telomere length. DNA repair expression assays were established by using cDNA arrays containing 96 DNA-repair genes and by Real Time Quantitative PCR. Results Our data indicated that telomere attrition was significantly associated with poor clinical outcome of patients ( P = 0.02), being this parameter a significant prognostic factor independent of tumour stage ( P = 0.012; relative risk = 1.887; 95% CI: 1.147–3.102). DNA-repair gene expression studies showed down regulation of DCLRE1C and GTF2H1 and a clear FLJ10858 up regulation in tumour tissues, as compared to controls. In addition, a number of genes related to DNA-repair were significantly down regulated in tumours that reactivated telomerase ( DCLRE1C , GTF2H1 , PARP-3 , MLH1 , and TRF2 ). Conclusions Telomere shortening emerged as a poor clinical evolution parameter in NSCLC. Moreover, results from this work suggest a relationship between the loss of several DNA repair genes and telomerase activity, which may be of relevance in the pathogenesis of non-small lung cancer.</description><identifier>ISSN: 0169-5002</identifier><identifier>EISSN: 1872-8332</identifier><identifier>DOI: 10.1016/j.lungcan.2007.11.001</identifier><identifier>PMID: 18077053</identifier><identifier>CODEN: LUCAE5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Adaptor Proteins, Signal Transducing - genetics ; Adult ; Aged ; Aged, 80 and over ; Biological and medical sciences ; Carcinoma, Non-Small-Cell Lung - diagnosis ; Carcinoma, Non-Small-Cell Lung - enzymology ; Carcinoma, Non-Small-Cell Lung - genetics ; Cell Cycle Proteins - genetics ; Clinical outcome ; DNA Repair ; DNA Repair Enzymes - genetics ; DNA repair factors ; DNA-Binding Proteins ; Endonucleases ; Female ; Hematology, Oncology and Palliative Medicine ; Humans ; Lung Neoplasms - diagnosis ; Lung Neoplasms - enzymology ; Lung Neoplasms - genetics ; Male ; Medical sciences ; Middle Aged ; MutL Protein Homolog 1 ; N-Glycosyl Hydrolases - genetics ; Non-small cell lung cancer ; Nuclear Proteins - genetics ; Phosphoproteins - genetics ; Pneumology ; Poly(ADP-ribose) Polymerases - genetics ; Prognosis ; Pulmonary/Respiratory ; Telomerase - genetics ; Telomerase activity ; Telomere - enzymology ; Telomere - genetics ; Telomere function ; Telomere shortening ; Telomere-binding proteins ; Telomeric Repeat Binding Protein 2 - genetics ; Transcription Factor TFIIH ; Transcription Factors, TFII - genetics ; Tumors ; Tumors of the respiratory system and mediastinum</subject><ispartof>Lung cancer (Amsterdam, Netherlands), 2008-06, Vol.60 (3), p.416-425</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2007 Elsevier Ireland Ltd</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-52ef5f6d375298adf1fa90c56320fea3201c4e7c16db433049aee24511a9a063</citedby><cites>FETCH-LOGICAL-c448t-52ef5f6d375298adf1fa90c56320fea3201c4e7c16db433049aee24511a9a063</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0169500207006642$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20488670$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18077053$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Frías, Cristina</creatorcontrib><creatorcontrib>García-Aranda, Cristina</creatorcontrib><creatorcontrib>De Juan, Carmen</creatorcontrib><creatorcontrib>Morán, Alberto</creatorcontrib><creatorcontrib>Ortega, Paloma</creatorcontrib><creatorcontrib>Gómez, Ana</creatorcontrib><creatorcontrib>Hernando, Florentino</creatorcontrib><creatorcontrib>López-Asenjo, Jose-Antonio</creatorcontrib><creatorcontrib>Torres, Antonio-José</creatorcontrib><creatorcontrib>Benito, Manuel</creatorcontrib><creatorcontrib>Iniesta, Pilar</creatorcontrib><title>Telomere shortening is associated with poor prognosis and telomerase activity correlates with DNA repair impairment in non-small cell lung cancer</title><title>Lung cancer (Amsterdam, Netherlands)</title><addtitle>Lung Cancer</addtitle><description>Summary Background and purpose Telomere function and DNA damage response pathways are frequently inactivated in cancer. Moreover, some telomere-binding proteins have been implicated in DNA repair. The purpose of this work consists of evaluating the prognostic impact of telomere dysfunction and its relationship with DNA repair systems in non-small cell lung cancer (NSCLC). Patients and methods We analysed 83 NSCLCs and their corresponding control samples obtained from patients submitted to surgery. Telomere function was evaluated by determining telomerase activity and telomere length. DNA repair expression assays were established by using cDNA arrays containing 96 DNA-repair genes and by Real Time Quantitative PCR. Results Our data indicated that telomere attrition was significantly associated with poor clinical outcome of patients ( P = 0.02), being this parameter a significant prognostic factor independent of tumour stage ( P = 0.012; relative risk = 1.887; 95% CI: 1.147–3.102). DNA-repair gene expression studies showed down regulation of DCLRE1C and GTF2H1 and a clear FLJ10858 up regulation in tumour tissues, as compared to controls. In addition, a number of genes related to DNA-repair were significantly down regulated in tumours that reactivated telomerase ( DCLRE1C , GTF2H1 , PARP-3 , MLH1 , and TRF2 ). Conclusions Telomere shortening emerged as a poor clinical evolution parameter in NSCLC. Moreover, results from this work suggest a relationship between the loss of several DNA repair genes and telomerase activity, which may be of relevance in the pathogenesis of non-small lung cancer.</description><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Non-Small-Cell Lung - diagnosis</subject><subject>Carcinoma, Non-Small-Cell Lung - enzymology</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Clinical outcome</subject><subject>DNA Repair</subject><subject>DNA Repair Enzymes - genetics</subject><subject>DNA repair factors</subject><subject>DNA-Binding Proteins</subject><subject>Endonucleases</subject><subject>Female</subject><subject>Hematology, Oncology and Palliative Medicine</subject><subject>Humans</subject><subject>Lung Neoplasms - diagnosis</subject><subject>Lung Neoplasms - enzymology</subject><subject>Lung Neoplasms - genetics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>MutL Protein Homolog 1</subject><subject>N-Glycosyl Hydrolases - genetics</subject><subject>Non-small cell lung cancer</subject><subject>Nuclear Proteins - genetics</subject><subject>Phosphoproteins - genetics</subject><subject>Pneumology</subject><subject>Poly(ADP-ribose) Polymerases - genetics</subject><subject>Prognosis</subject><subject>Pulmonary/Respiratory</subject><subject>Telomerase - genetics</subject><subject>Telomerase activity</subject><subject>Telomere - enzymology</subject><subject>Telomere - genetics</subject><subject>Telomere function</subject><subject>Telomere shortening</subject><subject>Telomere-binding proteins</subject><subject>Telomeric Repeat Binding Protein 2 - genetics</subject><subject>Transcription Factor TFIIH</subject><subject>Transcription Factors, TFII - genetics</subject><subject>Tumors</subject><subject>Tumors of the respiratory system and mediastinum</subject><issn>0169-5002</issn><issn>1872-8332</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFksuO1DAQRS0EYpqBTwB5A7uEsvNwsgGNhqc0ggW9tzxOpcdNYjeuZFB_Bn-Mo0QgsWFTtfC59bhlxp4LyAWI-vUxH2Z_sMbnEkDlQuQA4gHbiUbJrCkK-ZDtEtdmFYC8YE-IjglQAtrH7EI0oBRUxY792uMQRozI6S7ECb3zB-6IG6JgnZmw4z_ddMdPIUR-iuHgAy3PvuPTqjSE3NjJ3bvpzG2IEYcko1X27ssVj3gyLnI3LmlEP3HnuQ8-o9EMA7eYwrILT8tYjE_Zo94MhM-2fMn2H97vrz9lN18_fr6-uslsWTZTVknsq77uClXJtjFdL3rTgq3qQkKPJkVhS1RW1N1tWRRQtgZRlpUQpjVQF5fs1Vo2LfVjRpr06GiZxXgMM2klainKWiawWkEbA1HEXp-iG008awF6OYU-6u0UejmFFkInp5PuxdZgvh2x-6vavE_Ayw0wZM3Qx7S-oz-chLJpagWJe7tymNy4dxg1WYfJqs5FtJPugvvvKG_-qWAH511q-h3PSMcwR5-s1kKT1KC_Lf9m-TagAOq6lMVvjE_Bvg</recordid><startdate>20080601</startdate><enddate>20080601</enddate><creator>Frías, Cristina</creator><creator>García-Aranda, Cristina</creator><creator>De Juan, Carmen</creator><creator>Morán, Alberto</creator><creator>Ortega, Paloma</creator><creator>Gómez, Ana</creator><creator>Hernando, Florentino</creator><creator>López-Asenjo, Jose-Antonio</creator><creator>Torres, Antonio-José</creator><creator>Benito, Manuel</creator><creator>Iniesta, Pilar</creator><general>Elsevier Ireland Ltd</general><general>Elsevier Science</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>20080601</creationdate><title>Telomere shortening is associated with poor prognosis and telomerase activity correlates with DNA repair impairment in non-small cell lung cancer</title><author>Frías, Cristina ; García-Aranda, Cristina ; De Juan, Carmen ; Morán, Alberto ; Ortega, Paloma ; Gómez, Ana ; Hernando, Florentino ; López-Asenjo, Jose-Antonio ; Torres, Antonio-José ; Benito, Manuel ; Iniesta, Pilar</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-52ef5f6d375298adf1fa90c56320fea3201c4e7c16db433049aee24511a9a063</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Non-Small-Cell Lung - diagnosis</topic><topic>Carcinoma, Non-Small-Cell Lung - enzymology</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Cell Cycle Proteins - genetics</topic><topic>Clinical outcome</topic><topic>DNA Repair</topic><topic>DNA Repair Enzymes - genetics</topic><topic>DNA repair factors</topic><topic>DNA-Binding Proteins</topic><topic>Endonucleases</topic><topic>Female</topic><topic>Hematology, Oncology and Palliative Medicine</topic><topic>Humans</topic><topic>Lung Neoplasms - diagnosis</topic><topic>Lung Neoplasms - enzymology</topic><topic>Lung Neoplasms - genetics</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>MutL Protein Homolog 1</topic><topic>N-Glycosyl Hydrolases - genetics</topic><topic>Non-small cell lung cancer</topic><topic>Nuclear Proteins - genetics</topic><topic>Phosphoproteins - genetics</topic><topic>Pneumology</topic><topic>Poly(ADP-ribose) Polymerases - genetics</topic><topic>Prognosis</topic><topic>Pulmonary/Respiratory</topic><topic>Telomerase - genetics</topic><topic>Telomerase activity</topic><topic>Telomere - enzymology</topic><topic>Telomere - genetics</topic><topic>Telomere function</topic><topic>Telomere shortening</topic><topic>Telomere-binding proteins</topic><topic>Telomeric Repeat Binding Protein 2 - genetics</topic><topic>Transcription Factor TFIIH</topic><topic>Transcription Factors, TFII - genetics</topic><topic>Tumors</topic><topic>Tumors of the respiratory system and mediastinum</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Frías, Cristina</creatorcontrib><creatorcontrib>García-Aranda, Cristina</creatorcontrib><creatorcontrib>De Juan, Carmen</creatorcontrib><creatorcontrib>Morán, Alberto</creatorcontrib><creatorcontrib>Ortega, Paloma</creatorcontrib><creatorcontrib>Gómez, Ana</creatorcontrib><creatorcontrib>Hernando, Florentino</creatorcontrib><creatorcontrib>López-Asenjo, Jose-Antonio</creatorcontrib><creatorcontrib>Torres, Antonio-José</creatorcontrib><creatorcontrib>Benito, Manuel</creatorcontrib><creatorcontrib>Iniesta, Pilar</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>Lung cancer (Amsterdam, Netherlands)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Frías, Cristina</au><au>García-Aranda, Cristina</au><au>De Juan, Carmen</au><au>Morán, Alberto</au><au>Ortega, Paloma</au><au>Gómez, Ana</au><au>Hernando, Florentino</au><au>López-Asenjo, Jose-Antonio</au><au>Torres, Antonio-José</au><au>Benito, Manuel</au><au>Iniesta, Pilar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Telomere shortening is associated with poor prognosis and telomerase activity correlates with DNA repair impairment in non-small cell lung cancer</atitle><jtitle>Lung cancer (Amsterdam, Netherlands)</jtitle><addtitle>Lung Cancer</addtitle><date>2008-06-01</date><risdate>2008</risdate><volume>60</volume><issue>3</issue><spage>416</spage><epage>425</epage><pages>416-425</pages><issn>0169-5002</issn><eissn>1872-8332</eissn><coden>LUCAE5</coden><abstract>Summary Background and purpose Telomere function and DNA damage response pathways are frequently inactivated in cancer. Moreover, some telomere-binding proteins have been implicated in DNA repair. The purpose of this work consists of evaluating the prognostic impact of telomere dysfunction and its relationship with DNA repair systems in non-small cell lung cancer (NSCLC). Patients and methods We analysed 83 NSCLCs and their corresponding control samples obtained from patients submitted to surgery. Telomere function was evaluated by determining telomerase activity and telomere length. DNA repair expression assays were established by using cDNA arrays containing 96 DNA-repair genes and by Real Time Quantitative PCR. Results Our data indicated that telomere attrition was significantly associated with poor clinical outcome of patients ( P = 0.02), being this parameter a significant prognostic factor independent of tumour stage ( P = 0.012; relative risk = 1.887; 95% CI: 1.147–3.102). DNA-repair gene expression studies showed down regulation of DCLRE1C and GTF2H1 and a clear FLJ10858 up regulation in tumour tissues, as compared to controls. In addition, a number of genes related to DNA-repair were significantly down regulated in tumours that reactivated telomerase ( DCLRE1C , GTF2H1 , PARP-3 , MLH1 , and TRF2 ). Conclusions Telomere shortening emerged as a poor clinical evolution parameter in NSCLC. Moreover, results from this work suggest a relationship between the loss of several DNA repair genes and telomerase activity, which may be of relevance in the pathogenesis of non-small lung cancer.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>18077053</pmid><doi>10.1016/j.lungcan.2007.11.001</doi><tpages>10</tpages></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing - genetics Adult Aged Aged, 80 and over Biological and medical sciences Carcinoma, Non-Small-Cell Lung - diagnosis Carcinoma, Non-Small-Cell Lung - enzymology Carcinoma, Non-Small-Cell Lung - genetics Cell Cycle Proteins - genetics Clinical outcome DNA Repair DNA Repair Enzymes - genetics DNA repair factors DNA-Binding Proteins Endonucleases Female Hematology, Oncology and Palliative Medicine Humans Lung Neoplasms - diagnosis Lung Neoplasms - enzymology Lung Neoplasms - genetics Male Medical sciences Middle Aged MutL Protein Homolog 1 N-Glycosyl Hydrolases - genetics Non-small cell lung cancer Nuclear Proteins - genetics Phosphoproteins - genetics Pneumology Poly(ADP-ribose) Polymerases - genetics Prognosis Pulmonary/Respiratory Telomerase - genetics Telomerase activity Telomere - enzymology Telomere - genetics Telomere function Telomere shortening Telomere-binding proteins Telomeric Repeat Binding Protein 2 - genetics Transcription Factor TFIIH Transcription Factors, TFII - genetics Tumors Tumors of the respiratory system and mediastinum |
| title | Telomere shortening is associated with poor prognosis and telomerase activity correlates with DNA repair impairment in non-small cell lung cancer |
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