Targeting the Phosphatidylinositol 3-Kinase Pathway in Multiple Myeloma
Multiple myeloma is a plasma cell neoplasm with a median survival of 3 to 5 years. Recent advances have improved patient outlook, but the disease remains incurable. Therefore, continued efforts to develop new therapies that target aberrant signaling pathways are needed. The phosphatidylinositol 3-ki...
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| Veröffentlicht in: | Clinical cancer research 2007-07, Vol.13 (13), p.3771-3775 |
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| container_title | Clinical cancer research |
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| creator | YOUNES, Hashem LELEU, Xavier HATJIHARISSI, Evdoxia MOREAU, Anne-Sophie HIDESHIMA, Teru RICHARDSON, Paul ANDERSON, Kenneth C GHOBRIAL, Irene M |
| description | Multiple myeloma is a plasma cell neoplasm with a median survival of 3 to 5 years. Recent advances have improved patient outlook,
but the disease remains incurable. Therefore, continued efforts to develop new therapies that target aberrant signaling pathways
are needed. The phosphatidylinositol 3-kinase pathway regulates apoptosis, cell cycle regulation, and tumor proliferation.
This pathway is constitutively activated in multiple myeloma and its inhibition induces apoptosis. Advances in understanding
the signaling cascades mediating proliferation and survival of multiple myeloma cells have markedly improved the treatment
of this disease. In this article, we review the role of the phosphatidylinositol 3-kinase/Akt pathway in the pathogenesis
of multiple myeloma and the potential therapeutic implications of targeting this pathway in the treatment of multiple myeloma. |
| doi_str_mv | 10.1158/1078-0432.CCR-06-2921 |
| format | Article |
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but the disease remains incurable. Therefore, continued efforts to develop new therapies that target aberrant signaling pathways
are needed. The phosphatidylinositol 3-kinase pathway regulates apoptosis, cell cycle regulation, and tumor proliferation.
This pathway is constitutively activated in multiple myeloma and its inhibition induces apoptosis. Advances in understanding
the signaling cascades mediating proliferation and survival of multiple myeloma cells have markedly improved the treatment
of this disease. In this article, we review the role of the phosphatidylinositol 3-kinase/Akt pathway in the pathogenesis
of multiple myeloma and the potential therapeutic implications of targeting this pathway in the treatment of multiple myeloma.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.CCR-06-2921</identifier><identifier>PMID: 17606706</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Antineoplastic agents ; Antineoplastic Agents - therapeutic use ; Apoptosis ; Biological and medical sciences ; Cell Cycle ; Cell Proliferation ; Enzyme Inhibitors - therapeutic use ; Gene Expression Regulation, Neoplastic ; Hematologic and hematopoietic diseases ; HSP90 Heat-Shock Proteins - metabolism ; Humans ; Immunodeficiencies. Immunoglobulinopathies ; Immunoglobulinopathies ; Immunopathology ; Interleukin-6 - metabolism ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Medical sciences ; Models, Biological ; multiple myeloma ; Multiple Myeloma - enzymology ; Multiple Myeloma - mortality ; Multiple Myeloma - therapy ; novel targets of therapy ; Pharmacology. Drug treatments ; Phosphatidylinositol 3-Kinases - metabolism ; PI3K ; Signal Transduction ; signaling pathways ; Treatment Outcome</subject><ispartof>Clinical cancer research, 2007-07, Vol.13 (13), p.3771-3775</ispartof><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c489t-a88e371730e2ea0cd03c52cb2f5a65a2bff239f0019af5589d9e9f31c415c3013</citedby><cites>FETCH-LOGICAL-c489t-a88e371730e2ea0cd03c52cb2f5a65a2bff239f0019af5589d9e9f31c415c3013</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3342,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18926040$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17606706$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>YOUNES, Hashem</creatorcontrib><creatorcontrib>LELEU, Xavier</creatorcontrib><creatorcontrib>HATJIHARISSI, Evdoxia</creatorcontrib><creatorcontrib>MOREAU, Anne-Sophie</creatorcontrib><creatorcontrib>HIDESHIMA, Teru</creatorcontrib><creatorcontrib>RICHARDSON, Paul</creatorcontrib><creatorcontrib>ANDERSON, Kenneth C</creatorcontrib><creatorcontrib>GHOBRIAL, Irene M</creatorcontrib><title>Targeting the Phosphatidylinositol 3-Kinase Pathway in Multiple Myeloma</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Multiple myeloma is a plasma cell neoplasm with a median survival of 3 to 5 years. Recent advances have improved patient outlook,
but the disease remains incurable. Therefore, continued efforts to develop new therapies that target aberrant signaling pathways
are needed. The phosphatidylinositol 3-kinase pathway regulates apoptosis, cell cycle regulation, and tumor proliferation.
This pathway is constitutively activated in multiple myeloma and its inhibition induces apoptosis. Advances in understanding
the signaling cascades mediating proliferation and survival of multiple myeloma cells have markedly improved the treatment
of this disease. In this article, we review the role of the phosphatidylinositol 3-kinase/Akt pathway in the pathogenesis
of multiple myeloma and the potential therapeutic implications of targeting this pathway in the treatment of multiple myeloma.</description><subject>Antineoplastic agents</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Cell Cycle</subject><subject>Cell Proliferation</subject><subject>Enzyme Inhibitors - therapeutic use</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Hematologic and hematopoietic diseases</subject><subject>HSP90 Heat-Shock Proteins - metabolism</subject><subject>Humans</subject><subject>Immunodeficiencies. Immunoglobulinopathies</subject><subject>Immunoglobulinopathies</subject><subject>Immunopathology</subject><subject>Interleukin-6 - metabolism</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Medical sciences</subject><subject>Models, Biological</subject><subject>multiple myeloma</subject><subject>Multiple Myeloma - enzymology</subject><subject>Multiple Myeloma - mortality</subject><subject>Multiple Myeloma - therapy</subject><subject>novel targets of therapy</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>PI3K</subject><subject>Signal Transduction</subject><subject>signaling pathways</subject><subject>Treatment Outcome</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkN9r2zAQgEXZWLtuf0KHX1bYg7uTZFnW4wj9RVs2RvcsLsop1lDsTHIo-e8nk5TCgQ7uO93dx9gFhyvOVfedg-5qaKS4Wix-19DWwgh-ws64UrqWolXvSv7KnLKPOf8F4A2H5gM75bqFVkN7xm6fMa1pCsO6mnqqfvVj3vY4hdU-hmHMYRpjJeuHMGAuVZz6F9xXYaiednEK20jV057iuMFP7L3HmOnz8T1nf26unxd39ePP2_vFj8faNZ2Zauw6kpprCSQIwa1AOiXcUniFrUKx9F5I48umBr1SnVkZMl5y13DlJHB5zi4P_27T-G9HebKbkB3FiAONu2zLUdqAggKqA-jSmHMib7cpbDDtLQc7G7SzHTvbscWghdbOBkvfl-OA3XJDq7euo7ICfD0CmB1Gn3BwIb9xnREtNPMC3w5cH9b9S0hkXSEpJcqEyfWWyzmk1lz-B8cYhxU</recordid><startdate>20070701</startdate><enddate>20070701</enddate><creator>YOUNES, Hashem</creator><creator>LELEU, Xavier</creator><creator>HATJIHARISSI, Evdoxia</creator><creator>MOREAU, Anne-Sophie</creator><creator>HIDESHIMA, Teru</creator><creator>RICHARDSON, Paul</creator><creator>ANDERSON, Kenneth C</creator><creator>GHOBRIAL, Irene M</creator><general>American Association for Cancer Research</general><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>7X8</scope></search><sort><creationdate>20070701</creationdate><title>Targeting the Phosphatidylinositol 3-Kinase Pathway in Multiple Myeloma</title><author>YOUNES, Hashem ; LELEU, Xavier ; HATJIHARISSI, Evdoxia ; MOREAU, Anne-Sophie ; HIDESHIMA, Teru ; RICHARDSON, Paul ; ANDERSON, Kenneth C ; GHOBRIAL, Irene M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c489t-a88e371730e2ea0cd03c52cb2f5a65a2bff239f0019af5589d9e9f31c415c3013</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Antineoplastic agents</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Cell Cycle</topic><topic>Cell Proliferation</topic><topic>Enzyme Inhibitors - therapeutic use</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Hematologic and hematopoietic diseases</topic><topic>HSP90 Heat-Shock Proteins - metabolism</topic><topic>Humans</topic><topic>Immunodeficiencies. Immunoglobulinopathies</topic><topic>Immunoglobulinopathies</topic><topic>Immunopathology</topic><topic>Interleukin-6 - metabolism</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Medical sciences</topic><topic>Models, Biological</topic><topic>multiple myeloma</topic><topic>Multiple Myeloma - enzymology</topic><topic>Multiple Myeloma - mortality</topic><topic>Multiple Myeloma - therapy</topic><topic>novel targets of therapy</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>PI3K</topic><topic>Signal Transduction</topic><topic>signaling pathways</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>YOUNES, Hashem</creatorcontrib><creatorcontrib>LELEU, Xavier</creatorcontrib><creatorcontrib>HATJIHARISSI, Evdoxia</creatorcontrib><creatorcontrib>MOREAU, Anne-Sophie</creatorcontrib><creatorcontrib>HIDESHIMA, Teru</creatorcontrib><creatorcontrib>RICHARDSON, Paul</creatorcontrib><creatorcontrib>ANDERSON, Kenneth C</creatorcontrib><creatorcontrib>GHOBRIAL, Irene M</creatorcontrib><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>MEDLINE - Academic</collection><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>YOUNES, Hashem</au><au>LELEU, Xavier</au><au>HATJIHARISSI, Evdoxia</au><au>MOREAU, Anne-Sophie</au><au>HIDESHIMA, Teru</au><au>RICHARDSON, Paul</au><au>ANDERSON, Kenneth C</au><au>GHOBRIAL, Irene M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Targeting the Phosphatidylinositol 3-Kinase Pathway in Multiple Myeloma</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2007-07-01</date><risdate>2007</risdate><volume>13</volume><issue>13</issue><spage>3771</spage><epage>3775</epage><pages>3771-3775</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><abstract>Multiple myeloma is a plasma cell neoplasm with a median survival of 3 to 5 years. Recent advances have improved patient outlook,
but the disease remains incurable. Therefore, continued efforts to develop new therapies that target aberrant signaling pathways
are needed. The phosphatidylinositol 3-kinase pathway regulates apoptosis, cell cycle regulation, and tumor proliferation.
This pathway is constitutively activated in multiple myeloma and its inhibition induces apoptosis. Advances in understanding
the signaling cascades mediating proliferation and survival of multiple myeloma cells have markedly improved the treatment
of this disease. In this article, we review the role of the phosphatidylinositol 3-kinase/Akt pathway in the pathogenesis
of multiple myeloma and the potential therapeutic implications of targeting this pathway in the treatment of multiple myeloma.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>17606706</pmid><doi>10.1158/1078-0432.CCR-06-2921</doi><tpages>5</tpages></addata></record> |
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| ispartof | Clinical cancer research, 2007-07, Vol.13 (13), p.3771-3775 |
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| source | MEDLINE; American Association for Cancer Research Journals; Alma/SFX Local Collection; EZB Electronic Journals Library |
| subjects | Antineoplastic agents Antineoplastic Agents - therapeutic use Apoptosis Biological and medical sciences Cell Cycle Cell Proliferation Enzyme Inhibitors - therapeutic use Gene Expression Regulation, Neoplastic Hematologic and hematopoietic diseases HSP90 Heat-Shock Proteins - metabolism Humans Immunodeficiencies. Immunoglobulinopathies Immunoglobulinopathies Immunopathology Interleukin-6 - metabolism Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical sciences Models, Biological multiple myeloma Multiple Myeloma - enzymology Multiple Myeloma - mortality Multiple Myeloma - therapy novel targets of therapy Pharmacology. Drug treatments Phosphatidylinositol 3-Kinases - metabolism PI3K Signal Transduction signaling pathways Treatment Outcome |
| title | Targeting the Phosphatidylinositol 3-Kinase Pathway in Multiple Myeloma |
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