Gene expression signatures associated with the resistance to imatinib
Imatinib (imatinib mesylate, STI-571, Gleevec) is a selective BCR-ABL tyrosine kinase inhibitor that has been used as a highly effective chemoagent for treating chronic myelogenous leukemia. However, the initial response to imatinib is often followed by the recurrence of a resistant form of the dise...
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| Veröffentlicht in: | Leukemia 2006-09, Vol.20 (9), p.1542-1550 |
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| creator | CHUNG, Y.-J KIM, T.-M KANG, H.-M KIM, J. W KIM, D.-W NAMKOONG, H KIM, H. K HA, S.-A KIM, S SHIN, S. M KIM, J.-H LEE, Y.-J |
| description | Imatinib (imatinib mesylate, STI-571, Gleevec) is a selective BCR-ABL tyrosine kinase inhibitor that has been used as a highly effective chemoagent for treating chronic myelogenous leukemia. However, the initial response to imatinib is often followed by the recurrence of a resistant form of the disease, which is major obstacle to many therapeutic modalities. The aim of this study was to identify the gene expression signatures that confer resistance to imatinib. A series of four resistant K562 sublines was established with different imatinib dosage (200, 400, 600 and 800 nM) and analyzed using microarray technology. The transcripts of the genes showing universal or dose-dependent expression changes across the resistant sublines were identified. The gene sets associated with the imatinib-resistance were also identified using gene set enrichment analysis. In the resistant K562 sublines, the transcription- and apoptosis-related expression signatures were upregulated, whereas those related to the protein and energy metabolism were downregulated. Several genes identified in this study such as IGF1 and RAB11A have the potential to become surrogate markers useful in a clinical evaluation of imatinib-resistant patients without BCR-ABL mutation. The expression signatures identified in this study provide insights into the mechanism of imatinib-resistance and are expected to facilitate the development of an effective diagnostic and therapeutic strategy. |
| doi_str_mv | 10.1038/sj.leu.2404310 |
| format | Article |
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The transcripts of the genes showing universal or dose-dependent expression changes across the resistant sublines were identified. The gene sets associated with the imatinib-resistance were also identified using gene set enrichment analysis. In the resistant K562 sublines, the transcription- and apoptosis-related expression signatures were upregulated, whereas those related to the protein and energy metabolism were downregulated. Several genes identified in this study such as IGF1 and RAB11A have the potential to become surrogate markers useful in a clinical evaluation of imatinib-resistant patients without BCR-ABL mutation. The expression signatures identified in this study provide insights into the mechanism of imatinib-resistance and are expected to facilitate the development of an effective diagnostic and therapeutic strategy.</description><identifier>ISSN: 0887-6924</identifier><identifier>EISSN: 1476-5551</identifier><identifier>DOI: 10.1038/sj.leu.2404310</identifier><identifier>PMID: 16855633</identifier><identifier>CODEN: LEUKED</identifier><language>eng</language><publisher>London: Nature Publishing</publisher><subject>Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; Apoptosis ; BCR-ABL protein ; Benzamides ; Biological and medical sciences ; Chronic myeloid leukemia ; DNA microarrays ; Drug dosages ; Drug Resistance, Neoplasm - genetics ; Energy metabolism ; Enzyme inhibitors ; Fusion protein ; Gene expression ; Gene Expression Profiling ; Gene set enrichment analysis ; Genes ; Genomes ; Hematologic and hematopoietic diseases ; Humans ; Hybridization ; Imatinib ; Imatinib Mesylate ; Insulin-like growth factor I ; K562 Cells ; Kinases ; Leukemia ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics ; Medical schools ; Medical sciences ; Medicine ; Mutation ; Myeloid leukemia ; Piperazines - pharmacology ; Piperazines - therapeutic use ; Polymerase Chain Reaction ; Protein turnover ; Protein-tyrosine kinase ; Pyrimidines - pharmacology ; Pyrimidines - therapeutic use ; RNA, Messenger - genetics ; Signatures ; Transcription ; Tyrosine</subject><ispartof>Leukemia, 2006-09, Vol.20 (9), p.1542-1550</ispartof><rights>2006 INIST-CNRS</rights><rights>COPYRIGHT 2006 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Sep 2006</rights><rights>Nature Publishing Group 2006.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c538t-30eb24b79d014db50007e5561444d8bf6195552475fc024dc12e714a4e8991253</citedby><cites>FETCH-LOGICAL-c538t-30eb24b79d014db50007e5561444d8bf6195552475fc024dc12e714a4e8991253</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,2728,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18066224$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16855633$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CHUNG, Y.-J</creatorcontrib><creatorcontrib>KIM, T.-M</creatorcontrib><creatorcontrib>KANG, H.-M</creatorcontrib><creatorcontrib>KIM, J. W</creatorcontrib><creatorcontrib>KIM, D.-W</creatorcontrib><creatorcontrib>NAMKOONG, H</creatorcontrib><creatorcontrib>KIM, H. K</creatorcontrib><creatorcontrib>HA, S.-A</creatorcontrib><creatorcontrib>KIM, S</creatorcontrib><creatorcontrib>SHIN, S. M</creatorcontrib><creatorcontrib>KIM, J.-H</creatorcontrib><creatorcontrib>LEE, Y.-J</creatorcontrib><title>Gene expression signatures associated with the resistance to imatinib</title><title>Leukemia</title><addtitle>Leukemia</addtitle><description>Imatinib (imatinib mesylate, STI-571, Gleevec) is a selective BCR-ABL tyrosine kinase inhibitor that has been used as a highly effective chemoagent for treating chronic myelogenous leukemia. However, the initial response to imatinib is often followed by the recurrence of a resistant form of the disease, which is major obstacle to many therapeutic modalities. The aim of this study was to identify the gene expression signatures that confer resistance to imatinib. A series of four resistant K562 sublines was established with different imatinib dosage (200, 400, 600 and 800 nM) and analyzed using microarray technology. The transcripts of the genes showing universal or dose-dependent expression changes across the resistant sublines were identified. The gene sets associated with the imatinib-resistance were also identified using gene set enrichment analysis. In the resistant K562 sublines, the transcription- and apoptosis-related expression signatures were upregulated, whereas those related to the protein and energy metabolism were downregulated. Several genes identified in this study such as IGF1 and RAB11A have the potential to become surrogate markers useful in a clinical evaluation of imatinib-resistant patients without BCR-ABL mutation. The expression signatures identified in this study provide insights into the mechanism of imatinib-resistance and are expected to facilitate the development of an effective diagnostic and therapeutic strategy.</description><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Apoptosis</subject><subject>BCR-ABL protein</subject><subject>Benzamides</subject><subject>Biological and medical sciences</subject><subject>Chronic myeloid leukemia</subject><subject>DNA microarrays</subject><subject>Drug dosages</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Energy metabolism</subject><subject>Enzyme inhibitors</subject><subject>Fusion protein</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene set enrichment analysis</subject><subject>Genes</subject><subject>Genomes</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Hybridization</subject><subject>Imatinib</subject><subject>Imatinib Mesylate</subject><subject>Insulin-like growth factor I</subject><subject>K562 Cells</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics</subject><subject>Medical schools</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Mutation</subject><subject>Myeloid leukemia</subject><subject>Piperazines - pharmacology</subject><subject>Piperazines - therapeutic use</subject><subject>Polymerase Chain Reaction</subject><subject>Protein turnover</subject><subject>Protein-tyrosine kinase</subject><subject>Pyrimidines - pharmacology</subject><subject>Pyrimidines - therapeutic use</subject><subject>RNA, Messenger - genetics</subject><subject>Signatures</subject><subject>Transcription</subject><subject>Tyrosine</subject><issn>0887-6924</issn><issn>1476-5551</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><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>eNp1kk1v1DAQhi0Eokvhyg0UgehtF3_bOVZVKUiVuMDZcpxJ16tsvGQcFf49jjawgIp8sDx-Zua15yXkJaMbRoV9j7tND9OGSyoFo4_Iikmj10op9pisqLVmrWsuz8gzxB2l86V-Ss6YtkppIVbk-gYGqOD7YQTEmIYK493g81SOlUdMIfoMbXUf87bKW6hKPGL2Q4AqpyrufY5DbJ6TJ53vEV4s-zn5-uH6y9XH9e3nm09Xl7froITNa0Gh4bIxdVuUtI2ilBooQpiUsrVNp1ldlHNpVBcol21gHAyTXoKta8aVOCcXx7qHMX2bALPbRwzQ936ANKHT1hhbU1PAt_-AuzSNQ9HmuJbKMEGpLtSb_1KcKil1LU-l7nwPLg5dyqMPc193yaxVggk-l9o8QJXVwj6GNEAXS_yvhIs_Erbg-7zF1E-5DAEfrBzGhDhC5w5j-ffxh2PUzR5wuHPFA27xQEl4vbxqavbQnvBl6AV4twAeg--7sYwz4omzVGvO55e_OnJHQ_wGfjX6Cd7evwE</recordid><startdate>20060901</startdate><enddate>20060901</enddate><creator>CHUNG, Y.-J</creator><creator>KIM, T.-M</creator><creator>KANG, H.-M</creator><creator>KIM, J. 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| ispartof | Leukemia, 2006-09, Vol.20 (9), p.1542-1550 |
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| source | MEDLINE; Nature; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Apoptosis BCR-ABL protein Benzamides Biological and medical sciences Chronic myeloid leukemia DNA microarrays Drug dosages Drug Resistance, Neoplasm - genetics Energy metabolism Enzyme inhibitors Fusion protein Gene expression Gene Expression Profiling Gene set enrichment analysis Genes Genomes Hematologic and hematopoietic diseases Humans Hybridization Imatinib Imatinib Mesylate Insulin-like growth factor I K562 Cells Kinases Leukemia Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics Medical schools Medical sciences Medicine Mutation Myeloid leukemia Piperazines - pharmacology Piperazines - therapeutic use Polymerase Chain Reaction Protein turnover Protein-tyrosine kinase Pyrimidines - pharmacology Pyrimidines - therapeutic use RNA, Messenger - genetics Signatures Transcription Tyrosine |
| title | Gene expression signatures associated with the resistance to imatinib |
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