Telomere maintenance and dysfunction predict recurrence in paediatric ependymoma
We have recently described the enzymatic subunit of telomerase (hTERT) as an important prognostic marker for paediatric ependymoma. Because of the lack of good, representative pre-clinical models for ependymoma, we took advantage of our large cohort of ependymoma patients, some with multiple recurre...
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| Veröffentlicht in: | British journal of cancer 2008-10, Vol.99 (7), p.1129-1135 |
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| creator | Tabori, U Wong, V Ma, J Shago, M Alon, N Rutka, J Bouffet, E Bartels, U Malkin, D Hawkins, C |
| description | We have recently described the enzymatic subunit of telomerase (hTERT) as an important prognostic marker for paediatric ependymoma. Because of the lack of good, representative pre-clinical models for ependymoma, we took advantage of our large cohort of ependymoma patients, some with multiple recurrences, to investigate telomere biology in these tumours. Our cohort consisted of 133 ependymomas from 83 paediatric patients and included 31 patients with recurrences. Clinical outcome was measured as overall survival, progression-free survival and response to therapy. In all 133 tumours, hTERT expression correlated with proliferative markers, including MIB-1 index (
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| doi_str_mv | 10.1038/sj.bjc.6604652 |
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| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2567068</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>69609201</sourcerecordid><originalsourceid>FETCH-LOGICAL-c569t-401a24d1239d31791c692fadf842c08a6742d25f5eaa584366f1c220dbfc4fb73</originalsourceid><addsrcrecordid>eNqNkd1rFDEUxYNY7Lb66psyCPVttklm8vUiSPGjUNCH-hyyyU3NMJNZkxlh_3uz7LjVQtGnkHt-99zkHoReErwmuJGXuVtvOrvmHLec0SdoRVhDayKpeIpWGGNRY0XxKTrLuStXhaV4hk6JFEq0TK3Q11voxwESVIMJcYJoooXKRFe5XfZztFMYY7VN4IKdqgR2Tgn2SChVU6pmSsFWsIXodsM4mOfoxJs-w4vlPEffPn64vfpc33z5dH31_qa2jKupbjExtHWENso1RChiuaLeOC9barE0XLTUUeYZGMNk23DuiaUUu423rd-I5hy9O_hu580AzkKckun1NoXBpJ0eTdB_KzF813fjT00ZF5jLYvB2MUjjjxnypIeQLfS9iTDOWXPF96sj_wSJamkjuPpPkDYFfPMA7MY5xbIuTZuSEhOcF2h9gGwac07gj38jWO-z17nTJXu9ZF8aXv-5kXt8CbsAFwtgsjW9TyXrkI8cxZJIwljhLg9cLlK8g3T_vEdHvzp0RDPNCY6Wv_VfI2jSZA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>230005766</pqid></control><display><type>article</type><title>Telomere maintenance and dysfunction predict recurrence in paediatric ependymoma</title><source>MEDLINE</source><source>Nature</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>Tabori, U ; Wong, V ; Ma, J ; Shago, M ; Alon, N ; Rutka, J ; Bouffet, E ; Bartels, U ; Malkin, D ; Hawkins, C</creator><creatorcontrib>Tabori, U ; Wong, V ; Ma, J ; Shago, M ; Alon, N ; Rutka, J ; Bouffet, E ; Bartels, U ; Malkin, D ; Hawkins, C</creatorcontrib><description>We have recently described the enzymatic subunit of telomerase (hTERT) as an important prognostic marker for paediatric ependymoma. Because of the lack of good, representative pre-clinical models for ependymoma, we took advantage of our large cohort of ependymoma patients, some with multiple recurrences, to investigate telomere biology in these tumours. Our cohort consisted of 133 ependymomas from 83 paediatric patients and included 31 patients with recurrences. Clinical outcome was measured as overall survival, progression-free survival and response to therapy. In all 133 tumours, hTERT expression correlated with proliferative markers, including MIB-1 index (
P
<0.0001) and mitotic index (
P
=0.005), as well as overall tumour grade (
P
=0.001), but not with other markers of anaplasia. There was no correlation between telomere length and hTERT expression or survival. Surprisingly, prior radiation or chemotherapy neither induced sustained DNA damage nor affected telomere maintenance in recurrent tumours. There was an inverse correlation between hTERT expression and telomere dysfunction as measured by
γ
H2AX expression (
P
=0.016). Combining
γ
H2AX and hTERT expressions could segregate tumours into three different survival groups (log rank,
P
<0.0001) such that those patients whose tumours expressed hTERT and showed no evidence of DNA damage had the worst outcome. This study emphasises the importance of telomere biology as a prognostic tool and telomerase inhibition as a therapeutic target for paediatric ependymoma. Furthermore, we have demonstrated that analysing tumours as they progress
in vivo
is a viable approach to studying tumour biology in humans.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/sj.bjc.6604652</identifier><identifier>PMID: 18797459</identifier><identifier>CODEN: BJCAAI</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Biological and medical sciences ; Biology ; Biomedical and Life Sciences ; Biomedicine ; Brain cancer ; Cancer Research ; Cancer therapies ; Central Nervous System Neoplasms - genetics ; Central Nervous System Neoplasms - pathology ; Central Nervous System Neoplasms - therapy ; Chemotherapy ; Child ; Cohort Studies ; DNA damage ; Drug Resistance ; Ependymoma - genetics ; Ependymoma - pathology ; Ependymoma - therapy ; Epidemiology ; Humans ; Immunohistochemistry ; Medical prognosis ; Medical research ; Medical sciences ; Metastasis ; Molecular Diagnostics ; Molecular Medicine ; Neurology ; Oncology ; Pathology ; Pediatrics ; Prognosis ; Radiation ; Recurrence ; Survival analysis ; Telomerase ; Telomere ; Tumors ; Tumors of the nervous system. Phacomatoses ; Yeast</subject><ispartof>British journal of cancer, 2008-10, Vol.99 (7), p.1129-1135</ispartof><rights>The Author(s) 2008</rights><rights>2008 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Oct 7, 2008</rights><rights>Copyright © 2008 Cancer Research UK 2008 Cancer Research UK</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c569t-401a24d1239d31791c692fadf842c08a6742d25f5eaa584366f1c220dbfc4fb73</citedby><cites>FETCH-LOGICAL-c569t-401a24d1239d31791c692fadf842c08a6742d25f5eaa584366f1c220dbfc4fb73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2567068/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2567068/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,729,782,786,887,2729,27931,27932,53798,53800</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20818155$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18797459$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tabori, U</creatorcontrib><creatorcontrib>Wong, V</creatorcontrib><creatorcontrib>Ma, J</creatorcontrib><creatorcontrib>Shago, M</creatorcontrib><creatorcontrib>Alon, N</creatorcontrib><creatorcontrib>Rutka, J</creatorcontrib><creatorcontrib>Bouffet, E</creatorcontrib><creatorcontrib>Bartels, U</creatorcontrib><creatorcontrib>Malkin, D</creatorcontrib><creatorcontrib>Hawkins, C</creatorcontrib><title>Telomere maintenance and dysfunction predict recurrence in paediatric ependymoma</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>We have recently described the enzymatic subunit of telomerase (hTERT) as an important prognostic marker for paediatric ependymoma. Because of the lack of good, representative pre-clinical models for ependymoma, we took advantage of our large cohort of ependymoma patients, some with multiple recurrences, to investigate telomere biology in these tumours. Our cohort consisted of 133 ependymomas from 83 paediatric patients and included 31 patients with recurrences. Clinical outcome was measured as overall survival, progression-free survival and response to therapy. In all 133 tumours, hTERT expression correlated with proliferative markers, including MIB-1 index (
P
<0.0001) and mitotic index (
P
=0.005), as well as overall tumour grade (
P
=0.001), but not with other markers of anaplasia. There was no correlation between telomere length and hTERT expression or survival. Surprisingly, prior radiation or chemotherapy neither induced sustained DNA damage nor affected telomere maintenance in recurrent tumours. There was an inverse correlation between hTERT expression and telomere dysfunction as measured by
γ
H2AX expression (
P
=0.016). Combining
γ
H2AX and hTERT expressions could segregate tumours into three different survival groups (log rank,
P
<0.0001) such that those patients whose tumours expressed hTERT and showed no evidence of DNA damage had the worst outcome. This study emphasises the importance of telomere biology as a prognostic tool and telomerase inhibition as a therapeutic target for paediatric ependymoma. Furthermore, we have demonstrated that analysing tumours as they progress
in vivo
is a viable approach to studying tumour biology in humans.</description><subject>Biological and medical sciences</subject><subject>Biology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain cancer</subject><subject>Cancer Research</subject><subject>Cancer therapies</subject><subject>Central Nervous System Neoplasms - genetics</subject><subject>Central Nervous System Neoplasms - pathology</subject><subject>Central Nervous System Neoplasms - therapy</subject><subject>Chemotherapy</subject><subject>Child</subject><subject>Cohort Studies</subject><subject>DNA damage</subject><subject>Drug Resistance</subject><subject>Ependymoma - genetics</subject><subject>Ependymoma - pathology</subject><subject>Ependymoma - therapy</subject><subject>Epidemiology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Medical prognosis</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Metastasis</subject><subject>Molecular Diagnostics</subject><subject>Molecular Medicine</subject><subject>Neurology</subject><subject>Oncology</subject><subject>Pathology</subject><subject>Pediatrics</subject><subject>Prognosis</subject><subject>Radiation</subject><subject>Recurrence</subject><subject>Survival analysis</subject><subject>Telomerase</subject><subject>Telomere</subject><subject>Tumors</subject><subject>Tumors of the nervous system. Phacomatoses</subject><subject>Yeast</subject><issn>0007-0920</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkd1rFDEUxYNY7Lb66psyCPVttklm8vUiSPGjUNCH-hyyyU3NMJNZkxlh_3uz7LjVQtGnkHt-99zkHoReErwmuJGXuVtvOrvmHLec0SdoRVhDayKpeIpWGGNRY0XxKTrLuStXhaV4hk6JFEq0TK3Q11voxwESVIMJcYJoooXKRFe5XfZztFMYY7VN4IKdqgR2Tgn2SChVU6pmSsFWsIXodsM4mOfoxJs-w4vlPEffPn64vfpc33z5dH31_qa2jKupbjExtHWENso1RChiuaLeOC9barE0XLTUUeYZGMNk23DuiaUUu423rd-I5hy9O_hu580AzkKckun1NoXBpJ0eTdB_KzF813fjT00ZF5jLYvB2MUjjjxnypIeQLfS9iTDOWXPF96sj_wSJamkjuPpPkDYFfPMA7MY5xbIuTZuSEhOcF2h9gGwac07gj38jWO-z17nTJXu9ZF8aXv-5kXt8CbsAFwtgsjW9TyXrkI8cxZJIwljhLg9cLlK8g3T_vEdHvzp0RDPNCY6Wv_VfI2jSZA</recordid><startdate>20081007</startdate><enddate>20081007</enddate><creator>Tabori, U</creator><creator>Wong, V</creator><creator>Ma, J</creator><creator>Shago, M</creator><creator>Alon, N</creator><creator>Rutka, J</creator><creator>Bouffet, E</creator><creator>Bartels, U</creator><creator>Malkin, D</creator><creator>Hawkins, C</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>3V.</scope><scope>7RV</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20081007</creationdate><title>Telomere maintenance and dysfunction predict recurrence in paediatric ependymoma</title><author>Tabori, U ; Wong, V ; Ma, J ; Shago, M ; Alon, N ; Rutka, J ; Bouffet, E ; Bartels, U ; Malkin, D ; Hawkins, C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c569t-401a24d1239d31791c692fadf842c08a6742d25f5eaa584366f1c220dbfc4fb73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Biological and medical sciences</topic><topic>Biology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain cancer</topic><topic>Cancer Research</topic><topic>Cancer therapies</topic><topic>Central Nervous System Neoplasms - genetics</topic><topic>Central Nervous System Neoplasms - pathology</topic><topic>Central Nervous System Neoplasms - therapy</topic><topic>Chemotherapy</topic><topic>Child</topic><topic>Cohort Studies</topic><topic>DNA damage</topic><topic>Drug Resistance</topic><topic>Ependymoma - genetics</topic><topic>Ependymoma - pathology</topic><topic>Ependymoma - therapy</topic><topic>Epidemiology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Medical prognosis</topic><topic>Medical research</topic><topic>Medical sciences</topic><topic>Metastasis</topic><topic>Molecular Diagnostics</topic><topic>Molecular Medicine</topic><topic>Neurology</topic><topic>Oncology</topic><topic>Pathology</topic><topic>Pediatrics</topic><topic>Prognosis</topic><topic>Radiation</topic><topic>Recurrence</topic><topic>Survival analysis</topic><topic>Telomerase</topic><topic>Telomere</topic><topic>Tumors</topic><topic>Tumors of the nervous system. Phacomatoses</topic><topic>Yeast</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tabori, U</creatorcontrib><creatorcontrib>Wong, V</creatorcontrib><creatorcontrib>Ma, J</creatorcontrib><creatorcontrib>Shago, M</creatorcontrib><creatorcontrib>Alon, N</creatorcontrib><creatorcontrib>Rutka, J</creatorcontrib><creatorcontrib>Bouffet, E</creatorcontrib><creatorcontrib>Bartels, U</creatorcontrib><creatorcontrib>Malkin, D</creatorcontrib><creatorcontrib>Hawkins, C</creatorcontrib><collection>Springer Nature OA/Free Journals</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>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</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>ProQuest Pharma Collection</collection><collection>Public Health 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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</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><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tabori, U</au><au>Wong, V</au><au>Ma, J</au><au>Shago, M</au><au>Alon, N</au><au>Rutka, J</au><au>Bouffet, E</au><au>Bartels, U</au><au>Malkin, D</au><au>Hawkins, C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Telomere maintenance and dysfunction predict recurrence in paediatric ependymoma</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>2008-10-07</date><risdate>2008</risdate><volume>99</volume><issue>7</issue><spage>1129</spage><epage>1135</epage><pages>1129-1135</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>We have recently described the enzymatic subunit of telomerase (hTERT) as an important prognostic marker for paediatric ependymoma. Because of the lack of good, representative pre-clinical models for ependymoma, we took advantage of our large cohort of ependymoma patients, some with multiple recurrences, to investigate telomere biology in these tumours. Our cohort consisted of 133 ependymomas from 83 paediatric patients and included 31 patients with recurrences. Clinical outcome was measured as overall survival, progression-free survival and response to therapy. In all 133 tumours, hTERT expression correlated with proliferative markers, including MIB-1 index (
P
<0.0001) and mitotic index (
P
=0.005), as well as overall tumour grade (
P
=0.001), but not with other markers of anaplasia. There was no correlation between telomere length and hTERT expression or survival. Surprisingly, prior radiation or chemotherapy neither induced sustained DNA damage nor affected telomere maintenance in recurrent tumours. There was an inverse correlation between hTERT expression and telomere dysfunction as measured by
γ
H2AX expression (
P
=0.016). Combining
γ
H2AX and hTERT expressions could segregate tumours into three different survival groups (log rank,
P
<0.0001) such that those patients whose tumours expressed hTERT and showed no evidence of DNA damage had the worst outcome. This study emphasises the importance of telomere biology as a prognostic tool and telomerase inhibition as a therapeutic target for paediatric ependymoma. Furthermore, we have demonstrated that analysing tumours as they progress
in vivo
is a viable approach to studying tumour biology in humans.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>18797459</pmid><doi>10.1038/sj.bjc.6604652</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Nature; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Biological and medical sciences Biology Biomedical and Life Sciences Biomedicine Brain cancer Cancer Research Cancer therapies Central Nervous System Neoplasms - genetics Central Nervous System Neoplasms - pathology Central Nervous System Neoplasms - therapy Chemotherapy Child Cohort Studies DNA damage Drug Resistance Ependymoma - genetics Ependymoma - pathology Ependymoma - therapy Epidemiology Humans Immunohistochemistry Medical prognosis Medical research Medical sciences Metastasis Molecular Diagnostics Molecular Medicine Neurology Oncology Pathology Pediatrics Prognosis Radiation Recurrence Survival analysis Telomerase Telomere Tumors Tumors of the nervous system. Phacomatoses Yeast |
| title | Telomere maintenance and dysfunction predict recurrence in paediatric ependymoma |
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