Absence of the MGMT protein as well as methylation of the MGMT promoter predict the sensitivity for temozolomide
Background: The DNA repair protein O 6 -methylguanine-DNA methyltransferase (MGMT) can cause resistance to the alkylating drug temozolomide (TMZ). The purpose of this study was to determine the relationship between the MGMT status, determined by means of several techniques and methods, and the cytot...
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| Veröffentlicht in: | British journal of cancer 2010-06, Vol.103 (1), p.29-35 |
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| creator | van Nifterik, K A van den Berg, J van der Meide, W F Ameziane, N Wedekind, L E Steenbergen, R D M Leenstra, S Lafleur, M V M Slotman, B J Stalpers, L J A Sminia, P |
| description | Background:
The DNA repair protein O
6
-methylguanine-DNA methyltransferase (MGMT) can cause resistance to the alkylating drug temozolomide (TMZ). The purpose of this study was to determine the relationship between the MGMT status, determined by means of several techniques and methods, and the cytotoxic response to TMZ in 11 glioblastoma multiforme (GBM) cell lines and 5 human tumour cell lines of other origins.
Methods:
Cell survival was analysed by clonogenic assay. The MGMT protein levels were assessed by western blot analysis. The
MGMT
promoter methylation levels were determined using methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) and quantitative real-time methylation-specific PCR (qMSP). On the basis of the results of these techniques, six GBM cell lines were selected and subjected to bisulphite sequencing.
Results:
The MGMT protein was detected in all TMZ-resistant cell lines, whereas no MGMT protein could be detected in cell lines that were TMZ sensitive. The MS-MLPA results were able to predict TMZ sensitivity in 9 out of 16 cell lines (56%). The qMSP results matched well with TMZ sensitivity in 11 out of 12 (92%) glioma cell lines. In addition, methylation as detected by bisulphite sequencing seemed to be predictive of TMZ sensitivity in all six cell lines analysed (100%).
Conclusion:
The MGMT protein expression more than
MGMT
promoter methylation status predicts the response to TMZ in human tumour cell lines. |
| doi_str_mv | 10.1038/sj.bjc.6605712 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2905289</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>745937676</sourcerecordid><originalsourceid>FETCH-LOGICAL-c584t-3829360ea1a4cb2da58b2648d4e51b95d26d59c0a65d5bbe72de3ac41065479f3</originalsourceid><addsrcrecordid>eNp1kc1v1DAQxS1ERZfClSOKkBCnbG0n_rogVRUUpFZcytly7EnXURIvtrdo-evxsku_pJ7G1vv5zYwfQu8IXhLcyNM0LLvBLjnHTBD6Ai0Ia2hNJBUv0QJjLGqsKD5Gr1MaylVhKV6hY4oZEQ0WC7Q-6xLMFqrQV3kF1dXF1XW1jiGDnyuTqt8wjrs6QV5tR5N9mJ-iU4FjOYDzNv9TimPy2d_6vK36EKsMU_gTxjB5B2_QUW_GBG8P9QT9_Prl-vxbffnj4vv52WVtmWxz3UiqGo7BENPajjrDZEd5K10LjHSKOcodUxYbzhzrOhDUQWNsSzBnrVB9c4I-733Xm24CZ2HO0Yx6Hf1k4lYH4_VjZfYrfRNuNVWYUamKwaeDQQy_NpCynnyy5TvMDGGTtGiZagQXvJAfnpBD2MS5bKcZFYpzSUiBlnvIxpBShP5uFIL1LkqdBl2i1Icoy4P3Dxe4w_9nV4CPB8Aka8Y-mtn6dM9RpXjLdp1P91wq0nwD8X68Z1r_BT71uOo</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>527966811</pqid></control><display><type>article</type><title>Absence of the MGMT protein as well as methylation of the MGMT promoter predict the sensitivity for temozolomide</title><source>MEDLINE</source><source>Nature Journals Online</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>SpringerLink Journals - AutoHoldings</source><creator>van Nifterik, K A ; van den Berg, J ; van der Meide, W F ; Ameziane, N ; Wedekind, L E ; Steenbergen, R D M ; Leenstra, S ; Lafleur, M V M ; Slotman, B J ; Stalpers, L J A ; Sminia, P</creator><creatorcontrib>van Nifterik, K A ; van den Berg, J ; van der Meide, W F ; Ameziane, N ; Wedekind, L E ; Steenbergen, R D M ; Leenstra, S ; Lafleur, M V M ; Slotman, B J ; Stalpers, L J A ; Sminia, P</creatorcontrib><description>Background:
The DNA repair protein O
6
-methylguanine-DNA methyltransferase (MGMT) can cause resistance to the alkylating drug temozolomide (TMZ). The purpose of this study was to determine the relationship between the MGMT status, determined by means of several techniques and methods, and the cytotoxic response to TMZ in 11 glioblastoma multiforme (GBM) cell lines and 5 human tumour cell lines of other origins.
Methods:
Cell survival was analysed by clonogenic assay. The MGMT protein levels were assessed by western blot analysis. The
MGMT
promoter methylation levels were determined using methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) and quantitative real-time methylation-specific PCR (qMSP). On the basis of the results of these techniques, six GBM cell lines were selected and subjected to bisulphite sequencing.
Results:
The MGMT protein was detected in all TMZ-resistant cell lines, whereas no MGMT protein could be detected in cell lines that were TMZ sensitive. The MS-MLPA results were able to predict TMZ sensitivity in 9 out of 16 cell lines (56%). The qMSP results matched well with TMZ sensitivity in 11 out of 12 (92%) glioma cell lines. In addition, methylation as detected by bisulphite sequencing seemed to be predictive of TMZ sensitivity in all six cell lines analysed (100%).
Conclusion:
The MGMT protein expression more than
MGMT
promoter methylation status predicts the response to TMZ in human tumour cell lines.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/sj.bjc.6605712</identifier><identifier>PMID: 20517307</identifier><identifier>CODEN: BJCAAI</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/67/1059/2326 ; 692/53/2423 ; 692/699/67 ; Antineoplastic Agents, Alkylating - pharmacology ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Brain cancer ; Cancer Research ; Cancer therapies ; Cell Line, Tumor ; Cell Survival - drug effects ; CpG Islands ; Cytotoxicity ; Dacarbazine - analogs & derivatives ; Dacarbazine - pharmacology ; DNA Methylation ; DNA Modification Methylases - genetics ; DNA repair ; DNA Repair Enzymes - genetics ; Drug Resistance ; Epidemiology ; Glioblastoma - drug therapy ; Glioblastoma - pathology ; Humans ; Medical research ; Medical sciences ; Molecular Medicine ; Neurology ; Nucleic Acid Amplification Techniques ; Oncology ; Promoter Regions, Genetic ; Protein expression ; Proteins ; Radiation therapy ; Translational Therapeutics ; Tumor Suppressor Proteins - genetics ; Tumors ; Tumors of the nervous system. Phacomatoses</subject><ispartof>British journal of cancer, 2010-06, Vol.103 (1), p.29-35</ispartof><rights>The Author(s) 2010</rights><rights>2015 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jun 29, 2010</rights><rights>Copyright © 2010 Cancer Research UK 2010 Cancer Research UK</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c584t-3829360ea1a4cb2da58b2648d4e51b95d26d59c0a65d5bbe72de3ac41065479f3</citedby><cites>FETCH-LOGICAL-c584t-3829360ea1a4cb2da58b2648d4e51b95d26d59c0a65d5bbe72de3ac41065479f3</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/PMC2905289/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2905289/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27923,27924,41487,42556,51318,53790,53792</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22996451$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20517307$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>van Nifterik, K A</creatorcontrib><creatorcontrib>van den Berg, J</creatorcontrib><creatorcontrib>van der Meide, W F</creatorcontrib><creatorcontrib>Ameziane, N</creatorcontrib><creatorcontrib>Wedekind, L E</creatorcontrib><creatorcontrib>Steenbergen, R D M</creatorcontrib><creatorcontrib>Leenstra, S</creatorcontrib><creatorcontrib>Lafleur, M V M</creatorcontrib><creatorcontrib>Slotman, B J</creatorcontrib><creatorcontrib>Stalpers, L J A</creatorcontrib><creatorcontrib>Sminia, P</creatorcontrib><title>Absence of the MGMT protein as well as methylation of the MGMT promoter predict the sensitivity for temozolomide</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>Background:
The DNA repair protein O
6
-methylguanine-DNA methyltransferase (MGMT) can cause resistance to the alkylating drug temozolomide (TMZ). The purpose of this study was to determine the relationship between the MGMT status, determined by means of several techniques and methods, and the cytotoxic response to TMZ in 11 glioblastoma multiforme (GBM) cell lines and 5 human tumour cell lines of other origins.
Methods:
Cell survival was analysed by clonogenic assay. The MGMT protein levels were assessed by western blot analysis. The
MGMT
promoter methylation levels were determined using methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) and quantitative real-time methylation-specific PCR (qMSP). On the basis of the results of these techniques, six GBM cell lines were selected and subjected to bisulphite sequencing.
Results:
The MGMT protein was detected in all TMZ-resistant cell lines, whereas no MGMT protein could be detected in cell lines that were TMZ sensitive. The MS-MLPA results were able to predict TMZ sensitivity in 9 out of 16 cell lines (56%). The qMSP results matched well with TMZ sensitivity in 11 out of 12 (92%) glioma cell lines. In addition, methylation as detected by bisulphite sequencing seemed to be predictive of TMZ sensitivity in all six cell lines analysed (100%).
Conclusion:
The MGMT protein expression more than
MGMT
promoter methylation status predicts the response to TMZ in human tumour cell lines.</description><subject>631/67/1059/2326</subject><subject>692/53/2423</subject><subject>692/699/67</subject><subject>Antineoplastic Agents, Alkylating - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain cancer</subject><subject>Cancer Research</subject><subject>Cancer therapies</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival - drug effects</subject><subject>CpG Islands</subject><subject>Cytotoxicity</subject><subject>Dacarbazine - analogs & derivatives</subject><subject>Dacarbazine - pharmacology</subject><subject>DNA Methylation</subject><subject>DNA Modification Methylases - genetics</subject><subject>DNA repair</subject><subject>DNA Repair Enzymes - genetics</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>Glioblastoma - drug therapy</subject><subject>Glioblastoma - pathology</subject><subject>Humans</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Molecular Medicine</subject><subject>Neurology</subject><subject>Nucleic Acid Amplification Techniques</subject><subject>Oncology</subject><subject>Promoter Regions, Genetic</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Radiation therapy</subject><subject>Translational Therapeutics</subject><subject>Tumor Suppressor Proteins - genetics</subject><subject>Tumors</subject><subject>Tumors of the nervous system. Phacomatoses</subject><issn>0007-0920</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</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>eNp1kc1v1DAQxS1ERZfClSOKkBCnbG0n_rogVRUUpFZcytly7EnXURIvtrdo-evxsku_pJ7G1vv5zYwfQu8IXhLcyNM0LLvBLjnHTBD6Ai0Ia2hNJBUv0QJjLGqsKD5Gr1MaylVhKV6hY4oZEQ0WC7Q-6xLMFqrQV3kF1dXF1XW1jiGDnyuTqt8wjrs6QV5tR5N9mJ-iU4FjOYDzNv9TimPy2d_6vK36EKsMU_gTxjB5B2_QUW_GBG8P9QT9_Prl-vxbffnj4vv52WVtmWxz3UiqGo7BENPajjrDZEd5K10LjHSKOcodUxYbzhzrOhDUQWNsSzBnrVB9c4I-733Xm24CZ2HO0Yx6Hf1k4lYH4_VjZfYrfRNuNVWYUamKwaeDQQy_NpCynnyy5TvMDGGTtGiZagQXvJAfnpBD2MS5bKcZFYpzSUiBlnvIxpBShP5uFIL1LkqdBl2i1Icoy4P3Dxe4w_9nV4CPB8Aka8Y-mtn6dM9RpXjLdp1P91wq0nwD8X68Z1r_BT71uOo</recordid><startdate>20100629</startdate><enddate>20100629</enddate><creator>van Nifterik, K A</creator><creator>van den Berg, J</creator><creator>van der Meide, W F</creator><creator>Ameziane, N</creator><creator>Wedekind, L E</creator><creator>Steenbergen, R D M</creator><creator>Leenstra, S</creator><creator>Lafleur, M V M</creator><creator>Slotman, B J</creator><creator>Stalpers, L J A</creator><creator>Sminia, P</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>5PM</scope></search><sort><creationdate>20100629</creationdate><title>Absence of the MGMT protein as well as methylation of the MGMT promoter predict the sensitivity for temozolomide</title><author>van Nifterik, K A ; van den Berg, J ; van der Meide, W F ; Ameziane, N ; Wedekind, L E ; Steenbergen, R D M ; Leenstra, S ; Lafleur, M V M ; Slotman, B J ; Stalpers, L J A ; Sminia, P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c584t-3829360ea1a4cb2da58b2648d4e51b95d26d59c0a65d5bbe72de3ac41065479f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>631/67/1059/2326</topic><topic>692/53/2423</topic><topic>692/699/67</topic><topic>Antineoplastic Agents, Alkylating - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain cancer</topic><topic>Cancer Research</topic><topic>Cancer therapies</topic><topic>Cell Line, Tumor</topic><topic>Cell Survival - drug effects</topic><topic>CpG Islands</topic><topic>Cytotoxicity</topic><topic>Dacarbazine - analogs & derivatives</topic><topic>Dacarbazine - pharmacology</topic><topic>DNA Methylation</topic><topic>DNA Modification Methylases - genetics</topic><topic>DNA repair</topic><topic>DNA Repair Enzymes - genetics</topic><topic>Drug Resistance</topic><topic>Epidemiology</topic><topic>Glioblastoma - drug therapy</topic><topic>Glioblastoma - pathology</topic><topic>Humans</topic><topic>Medical research</topic><topic>Medical sciences</topic><topic>Molecular Medicine</topic><topic>Neurology</topic><topic>Nucleic Acid Amplification Techniques</topic><topic>Oncology</topic><topic>Promoter Regions, Genetic</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Radiation therapy</topic><topic>Translational Therapeutics</topic><topic>Tumor Suppressor Proteins - genetics</topic><topic>Tumors</topic><topic>Tumors of the nervous system. Phacomatoses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>van Nifterik, K A</creatorcontrib><creatorcontrib>van den Berg, J</creatorcontrib><creatorcontrib>van der Meide, W F</creatorcontrib><creatorcontrib>Ameziane, N</creatorcontrib><creatorcontrib>Wedekind, L E</creatorcontrib><creatorcontrib>Steenbergen, R D M</creatorcontrib><creatorcontrib>Leenstra, S</creatorcontrib><creatorcontrib>Lafleur, M V M</creatorcontrib><creatorcontrib>Slotman, B J</creatorcontrib><creatorcontrib>Stalpers, L J A</creatorcontrib><creatorcontrib>Sminia, P</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>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>van Nifterik, K A</au><au>van den Berg, J</au><au>van der Meide, W F</au><au>Ameziane, N</au><au>Wedekind, L E</au><au>Steenbergen, R D M</au><au>Leenstra, S</au><au>Lafleur, M V M</au><au>Slotman, B J</au><au>Stalpers, L J A</au><au>Sminia, P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Absence of the MGMT protein as well as methylation of the MGMT promoter predict the sensitivity for temozolomide</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>2010-06-29</date><risdate>2010</risdate><volume>103</volume><issue>1</issue><spage>29</spage><epage>35</epage><pages>29-35</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>Background:
The DNA repair protein O
6
-methylguanine-DNA methyltransferase (MGMT) can cause resistance to the alkylating drug temozolomide (TMZ). The purpose of this study was to determine the relationship between the MGMT status, determined by means of several techniques and methods, and the cytotoxic response to TMZ in 11 glioblastoma multiforme (GBM) cell lines and 5 human tumour cell lines of other origins.
Methods:
Cell survival was analysed by clonogenic assay. The MGMT protein levels were assessed by western blot analysis. The
MGMT
promoter methylation levels were determined using methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) and quantitative real-time methylation-specific PCR (qMSP). On the basis of the results of these techniques, six GBM cell lines were selected and subjected to bisulphite sequencing.
Results:
The MGMT protein was detected in all TMZ-resistant cell lines, whereas no MGMT protein could be detected in cell lines that were TMZ sensitive. The MS-MLPA results were able to predict TMZ sensitivity in 9 out of 16 cell lines (56%). The qMSP results matched well with TMZ sensitivity in 11 out of 12 (92%) glioma cell lines. In addition, methylation as detected by bisulphite sequencing seemed to be predictive of TMZ sensitivity in all six cell lines analysed (100%).
Conclusion:
The MGMT protein expression more than
MGMT
promoter methylation status predicts the response to TMZ in human tumour cell lines.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>20517307</pmid><doi>10.1038/sj.bjc.6605712</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Nature Journals Online; EZB-FREE-00999 freely available EZB journals; PubMed Central; SpringerLink Journals - AutoHoldings |
| subjects | 631/67/1059/2326 692/53/2423 692/699/67 Antineoplastic Agents, Alkylating - pharmacology Biological and medical sciences Biomedical and Life Sciences Biomedicine Brain cancer Cancer Research Cancer therapies Cell Line, Tumor Cell Survival - drug effects CpG Islands Cytotoxicity Dacarbazine - analogs & derivatives Dacarbazine - pharmacology DNA Methylation DNA Modification Methylases - genetics DNA repair DNA Repair Enzymes - genetics Drug Resistance Epidemiology Glioblastoma - drug therapy Glioblastoma - pathology Humans Medical research Medical sciences Molecular Medicine Neurology Nucleic Acid Amplification Techniques Oncology Promoter Regions, Genetic Protein expression Proteins Radiation therapy Translational Therapeutics Tumor Suppressor Proteins - genetics Tumors Tumors of the nervous system. Phacomatoses |
| title | Absence of the MGMT protein as well as methylation of the MGMT promoter predict the sensitivity for temozolomide |
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