The rho-kinase inhibitors Y-27632 and fasudil act synergistically with imatinib to inhibit the expansion of ex vivo CD34(+) CML progenitor cells
Evidence from cell line-based studies indicates that rho-kinase may play a role in the leukaemic transformation of human cells mediated by the BCR/ABL tyrosine kinase, manifest clinically as chronic myeloid leukaemia (CML). We therefore employed two separate inhibitors, Y-27632 and fasudil, to inhib...
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| Veröffentlicht in: | Leukemia 2007-08, Vol.21 (8), p.1708-1714 |
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| creator | Burthem, J Rees-Unwin, K Mottram, R Adams, J Lucas, G S Spooncer, E Whetton, A D |
| description | Evidence from cell line-based studies indicates that rho-kinase may play a role in the leukaemic transformation of human cells mediated by the BCR/ABL tyrosine kinase, manifest clinically as chronic myeloid leukaemia (CML). We therefore employed two separate inhibitors, Y-27632 and fasudil, to inhibit the activity of rho-kinase against ex vivo CD34(+) cells collected from patients with CML. We compared the effects of rho-kinase inhibition in those cells with the effects of direct inhibition of BCR/ABL using the specific inhibitor imatinib. We found that inhibition of rho-kinase inhibited the effective proliferation, and reduced survival of CML progenitor cells. When combined with imatinib, rho-kinase inhibition added to the anti-proliferative and pro-apoptotic effects of the BCR/ABL inhibitor. Our studies may indicate therapeutic benefit in some cases for the combination of rho-kinase inhibitors with imatinib. |
| doi_str_mv | 10.1038/sj.leu.2404762 |
| format | Article |
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We therefore employed two separate inhibitors, Y-27632 and fasudil, to inhibit the activity of rho-kinase against ex vivo CD34(+) cells collected from patients with CML. We compared the effects of rho-kinase inhibition in those cells with the effects of direct inhibition of BCR/ABL using the specific inhibitor imatinib. We found that inhibition of rho-kinase inhibited the effective proliferation, and reduced survival of CML progenitor cells. When combined with imatinib, rho-kinase inhibition added to the anti-proliferative and pro-apoptotic effects of the BCR/ABL inhibitor. Our studies may indicate therapeutic benefit in some cases for the combination of rho-kinase inhibitors with imatinib.</description><identifier>ISSN: 0887-6924</identifier><identifier>EISSN: 1476-5551</identifier><identifier>DOI: 10.1038/sj.leu.2404762</identifier><identifier>PMID: 17554385</identifier><language>eng</language><publisher>England: Nature Publishing Group</publisher><subject>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives ; 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - therapeutic use ; Amides - therapeutic use ; Antigens, CD34 - metabolism ; Apoptosis ; BCR-ABL protein ; BCR-ABL1 gene ; Benzamides ; Cancer cells ; CD34 antigen ; Cell proliferation ; Cell Proliferation - drug effects ; Cells (biology) ; Chemical inhibitors ; Chronic myeloid leukemia ; Drug Synergism ; Drug therapy ; Drug therapy, Combination ; Enzyme Inhibitors - therapeutic use ; Fusion Proteins, bcr-abl ; Growth ; Health aspects ; Humans ; Imatinib ; Imatinib Mesylate ; Inhibitor drugs ; Inhibitors ; Intracellular Signaling Peptides and Proteins - antagonists & inhibitors ; Kinases ; Leukemia ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology ; Piperazines - therapeutic use ; Progenitor cells ; Protein Kinase Inhibitors - therapeutic use ; Protein-Serine-Threonine Kinases - antagonists & inhibitors ; Protein-tyrosine kinase ; Protein-Tyrosine Kinases - antagonists & inhibitors ; Protein-Tyrosine Kinases - metabolism ; Pyridines - therapeutic use ; Pyrimidines - therapeutic use ; rho-Associated Kinases ; Stem Cells ; Targeted cancer therapy ; Tumor Cells, Cultured - drug effects ; Tyrosine</subject><ispartof>Leukemia, 2007-08, Vol.21 (8), p.1708-1714</ispartof><rights>COPYRIGHT 2007 Nature Publishing Group</rights><rights>Nature Publishing Group 2007.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c459t-7fbe9f2ec3e831eedb004ae7f9c1b0e6baabf842381e98840c047349786c433a3</citedby><cites>FETCH-LOGICAL-c459t-7fbe9f2ec3e831eedb004ae7f9c1b0e6baabf842381e98840c047349786c433a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17554385$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Burthem, J</creatorcontrib><creatorcontrib>Rees-Unwin, K</creatorcontrib><creatorcontrib>Mottram, R</creatorcontrib><creatorcontrib>Adams, J</creatorcontrib><creatorcontrib>Lucas, G S</creatorcontrib><creatorcontrib>Spooncer, E</creatorcontrib><creatorcontrib>Whetton, A D</creatorcontrib><title>The rho-kinase inhibitors Y-27632 and fasudil act synergistically with imatinib to inhibit the expansion of ex vivo CD34(+) CML progenitor cells</title><title>Leukemia</title><addtitle>Leukemia</addtitle><description>Evidence from cell line-based studies indicates that rho-kinase may play a role in the leukaemic transformation of human cells mediated by the BCR/ABL tyrosine kinase, manifest clinically as chronic myeloid leukaemia (CML). We therefore employed two separate inhibitors, Y-27632 and fasudil, to inhibit the activity of rho-kinase against ex vivo CD34(+) cells collected from patients with CML. We compared the effects of rho-kinase inhibition in those cells with the effects of direct inhibition of BCR/ABL using the specific inhibitor imatinib. We found that inhibition of rho-kinase inhibited the effective proliferation, and reduced survival of CML progenitor cells. When combined with imatinib, rho-kinase inhibition added to the anti-proliferative and pro-apoptotic effects of the BCR/ABL inhibitor. Our studies may indicate therapeutic benefit in some cases for the combination of rho-kinase inhibitors with imatinib.</description><subject>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives</subject><subject>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - therapeutic use</subject><subject>Amides - therapeutic use</subject><subject>Antigens, CD34 - metabolism</subject><subject>Apoptosis</subject><subject>BCR-ABL protein</subject><subject>BCR-ABL1 gene</subject><subject>Benzamides</subject><subject>Cancer cells</subject><subject>CD34 antigen</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Cells (biology)</subject><subject>Chemical inhibitors</subject><subject>Chronic myeloid leukemia</subject><subject>Drug Synergism</subject><subject>Drug therapy</subject><subject>Drug therapy, Combination</subject><subject>Enzyme Inhibitors - therapeutic use</subject><subject>Fusion Proteins, 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Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Burthem, J</au><au>Rees-Unwin, K</au><au>Mottram, R</au><au>Adams, J</au><au>Lucas, G S</au><au>Spooncer, E</au><au>Whetton, A D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The rho-kinase inhibitors Y-27632 and fasudil act synergistically with imatinib to inhibit the expansion of ex vivo CD34(+) CML progenitor cells</atitle><jtitle>Leukemia</jtitle><addtitle>Leukemia</addtitle><date>2007-08-01</date><risdate>2007</risdate><volume>21</volume><issue>8</issue><spage>1708</spage><epage>1714</epage><pages>1708-1714</pages><issn>0887-6924</issn><eissn>1476-5551</eissn><abstract>Evidence from cell line-based studies indicates that rho-kinase may play a role in the leukaemic transformation of human cells mediated by the BCR/ABL tyrosine kinase, manifest clinically as chronic myeloid leukaemia (CML). We therefore employed two separate inhibitors, Y-27632 and fasudil, to inhibit the activity of rho-kinase against ex vivo CD34(+) cells collected from patients with CML. We compared the effects of rho-kinase inhibition in those cells with the effects of direct inhibition of BCR/ABL using the specific inhibitor imatinib. We found that inhibition of rho-kinase inhibited the effective proliferation, and reduced survival of CML progenitor cells. When combined with imatinib, rho-kinase inhibition added to the anti-proliferative and pro-apoptotic effects of the BCR/ABL inhibitor. Our studies may indicate therapeutic benefit in some cases for the combination of rho-kinase inhibitors with imatinib.</abstract><cop>England</cop><pub>Nature Publishing Group</pub><pmid>17554385</pmid><doi>10.1038/sj.leu.2404762</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Leukemia, 2007-08, Vol.21 (8), p.1708-1714 |
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| subjects | 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - therapeutic use Amides - therapeutic use Antigens, CD34 - metabolism Apoptosis BCR-ABL protein BCR-ABL1 gene Benzamides Cancer cells CD34 antigen Cell proliferation Cell Proliferation - drug effects Cells (biology) Chemical inhibitors Chronic myeloid leukemia Drug Synergism Drug therapy Drug therapy, Combination Enzyme Inhibitors - therapeutic use Fusion Proteins, bcr-abl Growth Health aspects Humans Imatinib Imatinib Mesylate Inhibitor drugs Inhibitors Intracellular Signaling Peptides and Proteins - antagonists & inhibitors Kinases Leukemia Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology Piperazines - therapeutic use Progenitor cells Protein Kinase Inhibitors - therapeutic use Protein-Serine-Threonine Kinases - antagonists & inhibitors Protein-tyrosine kinase Protein-Tyrosine Kinases - antagonists & inhibitors Protein-Tyrosine Kinases - metabolism Pyridines - therapeutic use Pyrimidines - therapeutic use rho-Associated Kinases Stem Cells Targeted cancer therapy Tumor Cells, Cultured - drug effects Tyrosine |
| title | The rho-kinase inhibitors Y-27632 and fasudil act synergistically with imatinib to inhibit the expansion of ex vivo CD34(+) CML progenitor cells |
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