Effects of Imatinib Mesylate on Renin–Angiotensin System (RAS) Activity during the Clinical Course of Chronic Myeloid Leukaemia
The renin–angiotensin system (RAS) is involved in cell growth, proliferation and differentiation in bone marrow in an autocrine–paracrine manner, and it modulates normal and neoplastic haematopoietic cell proliferation. This study aimed to assess expressions of the RAS components, renin, angiotensin...
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| Veröffentlicht in: | Journal of international medical research 2009-07, Vol.37 (4), p.1018-1028 |
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| creator | Sayitoglu, M Haznedaroğlu, IC Hatirnaz, O Erbilgin, Y Aksu, S Koca, E Adiguzel, C Bayik, M Akalin, I Gülbas, Z Akay, M Unal, A Kaynar, L Ovali, E Yilmaz, M Yenerel, M Dagdas, S Ozet, G Ar, C Aydin, Y Soysal, T Durgun, B Ozcebe, O Tukun, A Ilhan, O Ozbek, U |
| description | The renin–angiotensin system (RAS) is involved in cell growth, proliferation and differentiation in bone marrow in an autocrine–paracrine manner, and it modulates normal and neoplastic haematopoietic cell proliferation. This study aimed to assess expressions of the RAS components, renin, angiotensinogen and angiotensin-converting enzyme (ACE), during imatinib mesylate treatment of patients with chronic myeloid leukaemia (CML). Expressions of RAS components were studied in patients with CML at the time of diagnosis (n = 83) and at 3, 6 and 12 months after diagnosis (n = 35) by quantitative real-time polymerase chain reaction. De novo CML patients had increased ACE, angiotensinogen and renin mRNA levels and these expression levels decreased following administration of imatinib. The RAS activities were significantly different among Sokal risk groups of CML, highlighting the altered biological activity of RAS in neoplastic disorders. The results of this study confirm that haematopoietic RAS affects neoplastic cell production, which may be altered via administration of tyrosine kinase inhibitors such as imatinib mesylate. |
| doi_str_mv | 10.1177/147323000903700406 |
| format | Article |
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This study aimed to assess expressions of the RAS components, renin, angiotensinogen and angiotensin-converting enzyme (ACE), during imatinib mesylate treatment of patients with chronic myeloid leukaemia (CML). Expressions of RAS components were studied in patients with CML at the time of diagnosis (n = 83) and at 3, 6 and 12 months after diagnosis (n = 35) by quantitative real-time polymerase chain reaction. De novo CML patients had increased ACE, angiotensinogen and renin mRNA levels and these expression levels decreased following administration of imatinib. The RAS activities were significantly different among Sokal risk groups of CML, highlighting the altered biological activity of RAS in neoplastic disorders. The results of this study confirm that haematopoietic RAS affects neoplastic cell production, which may be altered via administration of tyrosine kinase inhibitors such as imatinib mesylate.</description><identifier>ISSN: 0300-0605</identifier><identifier>EISSN: 1473-2300</identifier><identifier>DOI: 10.1177/147323000903700406</identifier><identifier>PMID: 19761684</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Adolescent ; Adult ; Aged ; Aged, 80 and over ; Angiotensinogen - genetics ; Angiotensinogen - metabolism ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; Benzamides ; Bone Marrow - drug effects ; Bone Marrow - pathology ; Drug Therapy, Combination ; Female ; Gene Expression ; Humans ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - physiopathology ; Male ; Middle Aged ; Peptidyl-Dipeptidase A - genetics ; Peptidyl-Dipeptidase A - metabolism ; Piperazines - pharmacology ; Piperazines - therapeutic use ; Protein Kinase Inhibitors - pharmacology ; Protein Kinase Inhibitors - therapeutic use ; Pyrimidines - pharmacology ; Pyrimidines - therapeutic use ; Renin - genetics ; Renin - metabolism ; Renin-Angiotensin System - drug effects ; Renin-Angiotensin System - physiology ; Young Adult</subject><ispartof>Journal of international medical research, 2009-07, Vol.37 (4), p.1018-1028</ispartof><rights>2009 SAGE Publications</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c341t-772798ffc6a8283dc60873049ad100d8fe7f1dd9782a991f3710ff6a85c18793</citedby><cites>FETCH-LOGICAL-c341t-772798ffc6a8283dc60873049ad100d8fe7f1dd9782a991f3710ff6a85c18793</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/147323000903700406$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/147323000903700406$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,776,780,21945,27830,27901,27902,44921,45309</link.rule.ids><linktorsrc>$$Uhttps://journals.sagepub.com/doi/full/10.1177/147323000903700406?utm_source=summon&utm_medium=discovery-provider$$EView_record_in_SAGE_Publications$$FView_record_in_$$GSAGE_Publications</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19761684$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sayitoglu, M</creatorcontrib><creatorcontrib>Haznedaroğlu, IC</creatorcontrib><creatorcontrib>Hatirnaz, O</creatorcontrib><creatorcontrib>Erbilgin, Y</creatorcontrib><creatorcontrib>Aksu, S</creatorcontrib><creatorcontrib>Koca, E</creatorcontrib><creatorcontrib>Adiguzel, C</creatorcontrib><creatorcontrib>Bayik, M</creatorcontrib><creatorcontrib>Akalin, I</creatorcontrib><creatorcontrib>Gülbas, Z</creatorcontrib><creatorcontrib>Akay, M</creatorcontrib><creatorcontrib>Unal, A</creatorcontrib><creatorcontrib>Kaynar, L</creatorcontrib><creatorcontrib>Ovali, E</creatorcontrib><creatorcontrib>Yilmaz, M</creatorcontrib><creatorcontrib>Yenerel, M</creatorcontrib><creatorcontrib>Dagdas, S</creatorcontrib><creatorcontrib>Ozet, G</creatorcontrib><creatorcontrib>Ar, C</creatorcontrib><creatorcontrib>Aydin, Y</creatorcontrib><creatorcontrib>Soysal, T</creatorcontrib><creatorcontrib>Durgun, B</creatorcontrib><creatorcontrib>Ozcebe, O</creatorcontrib><creatorcontrib>Tukun, A</creatorcontrib><creatorcontrib>Ilhan, O</creatorcontrib><creatorcontrib>Ozbek, U</creatorcontrib><creatorcontrib>The Turkish CML Study Group</creatorcontrib><title>Effects of Imatinib Mesylate on Renin–Angiotensin System (RAS) Activity during the Clinical Course of Chronic Myeloid Leukaemia</title><title>Journal of international medical research</title><addtitle>J Int Med Res</addtitle><description>The renin–angiotensin system (RAS) is involved in cell growth, proliferation and differentiation in bone marrow in an autocrine–paracrine manner, and it modulates normal and neoplastic haematopoietic cell proliferation. This study aimed to assess expressions of the RAS components, renin, angiotensinogen and angiotensin-converting enzyme (ACE), during imatinib mesylate treatment of patients with chronic myeloid leukaemia (CML). Expressions of RAS components were studied in patients with CML at the time of diagnosis (n = 83) and at 3, 6 and 12 months after diagnosis (n = 35) by quantitative real-time polymerase chain reaction. De novo CML patients had increased ACE, angiotensinogen and renin mRNA levels and these expression levels decreased following administration of imatinib. The RAS activities were significantly different among Sokal risk groups of CML, highlighting the altered biological activity of RAS in neoplastic disorders. The results of this study confirm that haematopoietic RAS affects neoplastic cell production, which may be altered via administration of tyrosine kinase inhibitors such as imatinib mesylate.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Angiotensinogen - genetics</subject><subject>Angiotensinogen - metabolism</subject><subject>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</subject><subject>Benzamides</subject><subject>Bone Marrow - drug effects</subject><subject>Bone Marrow - pathology</subject><subject>Drug Therapy, Combination</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Humans</subject><subject>Imatinib Mesylate</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - physiopathology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Peptidyl-Dipeptidase A - genetics</subject><subject>Peptidyl-Dipeptidase A - metabolism</subject><subject>Piperazines - pharmacology</subject><subject>Piperazines - therapeutic use</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Protein Kinase Inhibitors - therapeutic use</subject><subject>Pyrimidines - pharmacology</subject><subject>Pyrimidines - therapeutic use</subject><subject>Renin - genetics</subject><subject>Renin - metabolism</subject><subject>Renin-Angiotensin System - drug effects</subject><subject>Renin-Angiotensin System - physiology</subject><subject>Young Adult</subject><issn>0300-0605</issn><issn>1473-2300</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kNFq2zAUhsXYWNNsL7CLoqvRXng5sh3JvgymXQspgyT3RpGPEnW21FpywXfbM_QN9yRVSKAXhV0d-Pn-D85PyDcGPxgTYsZykaUZAJSQCYAc-AcyOYTJIf1IJhBPAhzmZ-Tc-4eIpHyefiZnrBSc8SKfkL_XWqMKnjpN7zoZjDVbeo9-bGVA6ixdoTX235-Xhd0ZF9B6Y-l69AE7erlarK_oQgXzbMJIm6E3dkfDHmnVRo-SLa3c0Hs8yKt972JG70dsnWnoEoffEjsjv5BPWrYev57ulGxurjfVbbL89fOuWiwTleUsJEKkoiy0VlwWaZE1ikMhMshL2TCAptAoNGuaUhSpLEumM8FA6wjPFStEmU3J96P2sXdPA_pQd8YrbFtp0Q2-5oJzlsc9pyQ9gqp33veo68fedLIfawb1Yff6_e6xdHGyD9sOm7fKaegIzI6AlzusH-IsNj77P-UrMT-Lmg</recordid><startdate>20090701</startdate><enddate>20090701</enddate><creator>Sayitoglu, M</creator><creator>Haznedaroğlu, IC</creator><creator>Hatirnaz, O</creator><creator>Erbilgin, Y</creator><creator>Aksu, S</creator><creator>Koca, E</creator><creator>Adiguzel, C</creator><creator>Bayik, M</creator><creator>Akalin, I</creator><creator>Gülbas, Z</creator><creator>Akay, M</creator><creator>Unal, A</creator><creator>Kaynar, L</creator><creator>Ovali, E</creator><creator>Yilmaz, M</creator><creator>Yenerel, M</creator><creator>Dagdas, S</creator><creator>Ozet, G</creator><creator>Ar, C</creator><creator>Aydin, Y</creator><creator>Soysal, T</creator><creator>Durgun, B</creator><creator>Ozcebe, O</creator><creator>Tukun, A</creator><creator>Ilhan, O</creator><creator>Ozbek, U</creator><general>SAGE Publications</general><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>20090701</creationdate><title>Effects of Imatinib Mesylate on Renin–Angiotensin System (RAS) Activity during the Clinical Course of Chronic Myeloid Leukaemia</title><author>Sayitoglu, M ; Haznedaroğlu, IC ; Hatirnaz, O ; Erbilgin, Y ; Aksu, S ; Koca, E ; Adiguzel, C ; Bayik, M ; Akalin, I ; Gülbas, Z ; Akay, M ; Unal, A ; Kaynar, L ; Ovali, E ; Yilmaz, M ; Yenerel, M ; Dagdas, S ; Ozet, G ; Ar, C ; Aydin, Y ; Soysal, T ; Durgun, B ; Ozcebe, O ; Tukun, A ; Ilhan, O ; Ozbek, U</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c341t-772798ffc6a8283dc60873049ad100d8fe7f1dd9782a991f3710ff6a85c18793</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Angiotensinogen - genetics</topic><topic>Angiotensinogen - metabolism</topic><topic>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</topic><topic>Benzamides</topic><topic>Bone Marrow - drug effects</topic><topic>Bone Marrow - pathology</topic><topic>Drug Therapy, Combination</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Humans</topic><topic>Imatinib Mesylate</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - physiopathology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Peptidyl-Dipeptidase A - genetics</topic><topic>Peptidyl-Dipeptidase A - metabolism</topic><topic>Piperazines - pharmacology</topic><topic>Piperazines - therapeutic use</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>Protein Kinase Inhibitors - therapeutic use</topic><topic>Pyrimidines - pharmacology</topic><topic>Pyrimidines - therapeutic use</topic><topic>Renin - genetics</topic><topic>Renin - metabolism</topic><topic>Renin-Angiotensin System - drug effects</topic><topic>Renin-Angiotensin System - physiology</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sayitoglu, M</creatorcontrib><creatorcontrib>Haznedaroğlu, IC</creatorcontrib><creatorcontrib>Hatirnaz, O</creatorcontrib><creatorcontrib>Erbilgin, Y</creatorcontrib><creatorcontrib>Aksu, S</creatorcontrib><creatorcontrib>Koca, E</creatorcontrib><creatorcontrib>Adiguzel, C</creatorcontrib><creatorcontrib>Bayik, M</creatorcontrib><creatorcontrib>Akalin, I</creatorcontrib><creatorcontrib>Gülbas, Z</creatorcontrib><creatorcontrib>Akay, M</creatorcontrib><creatorcontrib>Unal, A</creatorcontrib><creatorcontrib>Kaynar, L</creatorcontrib><creatorcontrib>Ovali, E</creatorcontrib><creatorcontrib>Yilmaz, M</creatorcontrib><creatorcontrib>Yenerel, M</creatorcontrib><creatorcontrib>Dagdas, S</creatorcontrib><creatorcontrib>Ozet, G</creatorcontrib><creatorcontrib>Ar, C</creatorcontrib><creatorcontrib>Aydin, Y</creatorcontrib><creatorcontrib>Soysal, T</creatorcontrib><creatorcontrib>Durgun, B</creatorcontrib><creatorcontrib>Ozcebe, O</creatorcontrib><creatorcontrib>Tukun, A</creatorcontrib><creatorcontrib>Ilhan, O</creatorcontrib><creatorcontrib>Ozbek, U</creatorcontrib><creatorcontrib>The Turkish CML Study Group</creatorcontrib><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>Journal of international medical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Sayitoglu, M</au><au>Haznedaroğlu, IC</au><au>Hatirnaz, O</au><au>Erbilgin, Y</au><au>Aksu, S</au><au>Koca, E</au><au>Adiguzel, C</au><au>Bayik, M</au><au>Akalin, I</au><au>Gülbas, Z</au><au>Akay, M</au><au>Unal, A</au><au>Kaynar, L</au><au>Ovali, E</au><au>Yilmaz, M</au><au>Yenerel, M</au><au>Dagdas, S</au><au>Ozet, G</au><au>Ar, C</au><au>Aydin, Y</au><au>Soysal, T</au><au>Durgun, B</au><au>Ozcebe, O</au><au>Tukun, A</au><au>Ilhan, O</au><au>Ozbek, U</au><aucorp>The Turkish CML Study Group</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of Imatinib Mesylate on Renin–Angiotensin System (RAS) Activity during the Clinical Course of Chronic Myeloid Leukaemia</atitle><jtitle>Journal of international medical research</jtitle><addtitle>J Int Med Res</addtitle><date>2009-07-01</date><risdate>2009</risdate><volume>37</volume><issue>4</issue><spage>1018</spage><epage>1028</epage><pages>1018-1028</pages><issn>0300-0605</issn><eissn>1473-2300</eissn><abstract>The renin–angiotensin system (RAS) is involved in cell growth, proliferation and differentiation in bone marrow in an autocrine–paracrine manner, and it modulates normal and neoplastic haematopoietic cell proliferation. This study aimed to assess expressions of the RAS components, renin, angiotensinogen and angiotensin-converting enzyme (ACE), during imatinib mesylate treatment of patients with chronic myeloid leukaemia (CML). Expressions of RAS components were studied in patients with CML at the time of diagnosis (n = 83) and at 3, 6 and 12 months after diagnosis (n = 35) by quantitative real-time polymerase chain reaction. De novo CML patients had increased ACE, angiotensinogen and renin mRNA levels and these expression levels decreased following administration of imatinib. The RAS activities were significantly different among Sokal risk groups of CML, highlighting the altered biological activity of RAS in neoplastic disorders. The results of this study confirm that haematopoietic RAS affects neoplastic cell production, which may be altered via administration of tyrosine kinase inhibitors such as imatinib mesylate.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>19761684</pmid><doi>10.1177/147323000903700406</doi><tpages>11</tpages></addata></record> |
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| subjects | Adolescent Adult Aged Aged, 80 and over Angiotensinogen - genetics Angiotensinogen - metabolism Antineoplastic Combined Chemotherapy Protocols - therapeutic use Benzamides Bone Marrow - drug effects Bone Marrow - pathology Drug Therapy, Combination Female Gene Expression Humans Imatinib Mesylate Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism Leukemia, Myelogenous, Chronic, BCR-ABL Positive - physiopathology Male Middle Aged Peptidyl-Dipeptidase A - genetics Peptidyl-Dipeptidase A - metabolism Piperazines - pharmacology Piperazines - therapeutic use Protein Kinase Inhibitors - pharmacology Protein Kinase Inhibitors - therapeutic use Pyrimidines - pharmacology Pyrimidines - therapeutic use Renin - genetics Renin - metabolism Renin-Angiotensin System - drug effects Renin-Angiotensin System - physiology Young Adult |
| title | Effects of Imatinib Mesylate on Renin–Angiotensin System (RAS) Activity during the Clinical Course of Chronic Myeloid Leukaemia |
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