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How I treat patients who mobilize hematopoietic stem cells poorly
Transplantation with 2-5 × 106 mobilized CD34+cells/kg body weight lowers transplantation costs and mortality. Mobilization is most commonly performed with recombinant human G-CSF with or without chemotherapy, but a proportion of patients/donors fail to mobilize sufficient cells. BM disease, prior t...
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| Published in: | Blood 2011-10, Vol.118 (17), p.4530-4540 |
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| creator | To, L. Bik Levesque, Jean-Pierre Herbert, Kirsten E. |
| description | Transplantation with 2-5 × 106 mobilized CD34+cells/kg body weight lowers transplantation costs and mortality. Mobilization is most commonly performed with recombinant human G-CSF with or without chemotherapy, but a proportion of patients/donors fail to mobilize sufficient cells. BM disease, prior treatment, and age are factors influencing mobilization, but genetics also contributes. Mobilization may fail because of the changes affecting the HSC/progenitor cell/BM niche integrity and chemotaxis. Poor mobilization affects patient outcome and increases resource use. Until recently increasing G-CSF dose and adding SCF have been used in poor mobilizers with limited success. However, plerixafor through its rapid direct blockage of the CXCR4/CXCL12 chemotaxis pathway and synergy with G-CSF and chemotherapy has become a new and important agent for mobilization. Its efficacy in upfront and failed mobilizers is well established. To maximize HSC harvest in poor mobilizers the clinician needs to optimize current mobilization protocols and to integrate novel agents such as plerixafor. These include when to mobilize in relation to chemotherapy, how to schedule and perform apheresis, how to identify poor mobilizers, and what are the criteria for preemptive and immediate salvage use of plerixafor. |
| doi_str_mv | 10.1182/blood-2011-06-318220 |
| format | article |
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However, plerixafor through its rapid direct blockage of the CXCR4/CXCL12 chemotaxis pathway and synergy with G-CSF and chemotherapy has become a new and important agent for mobilization. Its efficacy in upfront and failed mobilizers is well established. To maximize HSC harvest in poor mobilizers the clinician needs to optimize current mobilization protocols and to integrate novel agents such as plerixafor. These include when to mobilize in relation to chemotherapy, how to schedule and perform apheresis, how to identify poor mobilizers, and what are the criteria for preemptive and immediate salvage use of plerixafor.</description><identifier>ISSN: 0006-4971</identifier><identifier>EISSN: 1528-0020</identifier><identifier>DOI: 10.1182/blood-2011-06-318220</identifier><identifier>PMID: 21832280</identifier><language>eng</language><publisher>Washington, DC: Elsevier Inc</publisher><subject>Anemia, Aplastic ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Biological and medical sciences ; Bone Marrow Diseases ; Bone Marrow Failure Disorders ; Bone marrow, stem cells transplantation. Graft versus host reaction ; Hematologic and hematopoietic diseases ; Hematologic Neoplasms - therapy ; Hematopoietic Stem Cell Mobilization - methods ; Hematopoietic Stem Cell Transplantation - methods ; Hematopoietic Stem Cells - pathology ; Hematopoietic Stem Cells - physiology ; Hemoglobinuria, Paroxysmal - therapy ; Humans ; Medical sciences ; Models, Biological ; Transfusions. Complications. Transfusion reactions. 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Bik</creatorcontrib><creatorcontrib>Levesque, Jean-Pierre</creatorcontrib><creatorcontrib>Herbert, Kirsten E.</creatorcontrib><title>How I treat patients who mobilize hematopoietic stem cells poorly</title><title>Blood</title><addtitle>Blood</addtitle><description>Transplantation with 2-5 × 106 mobilized CD34+cells/kg body weight lowers transplantation costs and mortality. Mobilization is most commonly performed with recombinant human G-CSF with or without chemotherapy, but a proportion of patients/donors fail to mobilize sufficient cells. BM disease, prior treatment, and age are factors influencing mobilization, but genetics also contributes. Mobilization may fail because of the changes affecting the HSC/progenitor cell/BM niche integrity and chemotaxis. Poor mobilization affects patient outcome and increases resource use. Until recently increasing G-CSF dose and adding SCF have been used in poor mobilizers with limited success. However, plerixafor through its rapid direct blockage of the CXCR4/CXCL12 chemotaxis pathway and synergy with G-CSF and chemotherapy has become a new and important agent for mobilization. Its efficacy in upfront and failed mobilizers is well established. To maximize HSC harvest in poor mobilizers the clinician needs to optimize current mobilization protocols and to integrate novel agents such as plerixafor. These include when to mobilize in relation to chemotherapy, how to schedule and perform apheresis, how to identify poor mobilizers, and what are the criteria for preemptive and immediate salvage use of plerixafor.</description><subject>Anemia, Aplastic</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Biological and medical sciences</subject><subject>Bone Marrow Diseases</subject><subject>Bone Marrow Failure Disorders</subject><subject>Bone marrow, stem cells transplantation. Graft versus host reaction</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hematologic Neoplasms - therapy</subject><subject>Hematopoietic Stem Cell Mobilization - methods</subject><subject>Hematopoietic Stem Cell Transplantation - methods</subject><subject>Hematopoietic Stem Cells - pathology</subject><subject>Hematopoietic Stem Cells - physiology</subject><subject>Hemoglobinuria, Paroxysmal - therapy</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Models, Biological</subject><subject>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</subject><subject>Transplantation Conditioning - methods</subject><subject>Treatment Failure</subject><issn>0006-4971</issn><issn>1528-0020</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNp9kMFO3DAQhq2Kqmyhb1AhXxCntDO2EyeXSghBQULqpZwtx5kIV8k6tb0gePp6uwvcOI00883Mr4-xrwjfEFvxvZ9CGCoBiBU0lSwtAR_YCmvRVgACDtgKoExUp_GQfU7pDwAqKepP7FBgK4VoYcXOr8Mjv-E5ks18sdnTOif-eB_4HHo_-Wfi9zTbHJbgKXvHU6aZO5qmxJcQ4vR0zD6Odkr0ZV-P2N3V5e-L6-r218-bi_PbytUgc9U0GtXYy1oKtF2viTotgBz22I5StQOSk7XQSpLVriE9jEOrbV-GoKgf5RE7291dYvi7oZTN7NM2iF1T2CTTAQIohK6Qake6GFKKNJol-tnGJ4Ngtu7Mf3dm685AY3buytrJ_sGmn2l4XXqRVYDTPWCTs9MY7dr59MYpDW0DWLgfO46KjgdP0SRXvDoafCSXzRD8-0n-AfStjNI</recordid><startdate>20111027</startdate><enddate>20111027</enddate><creator>To, L. Bik</creator><creator>Levesque, Jean-Pierre</creator><creator>Herbert, Kirsten E.</creator><general>Elsevier Inc</general><general>Americain Society of Hematology</general><scope>6I.</scope><scope>AAFTH</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>7X8</scope></search><sort><creationdate>20111027</creationdate><title>How I treat patients who mobilize hematopoietic stem cells poorly</title><author>To, L. Bik ; Levesque, Jean-Pierre ; Herbert, Kirsten E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-66714fb35321a9b7ee9720ec1b18f348d1ec352743ea7c6e7dfd87ab8f304ebf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Anemia, Aplastic</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Biological and medical sciences</topic><topic>Bone Marrow Diseases</topic><topic>Bone Marrow Failure Disorders</topic><topic>Bone marrow, stem cells transplantation. Graft versus host reaction</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hematologic Neoplasms - therapy</topic><topic>Hematopoietic Stem Cell Mobilization - methods</topic><topic>Hematopoietic Stem Cell Transplantation - methods</topic><topic>Hematopoietic Stem Cells - pathology</topic><topic>Hematopoietic Stem Cells - physiology</topic><topic>Hemoglobinuria, Paroxysmal - therapy</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Models, Biological</topic><topic>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</topic><topic>Transplantation Conditioning - methods</topic><topic>Treatment Failure</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>To, L. Bik</creatorcontrib><creatorcontrib>Levesque, Jean-Pierre</creatorcontrib><creatorcontrib>Herbert, Kirsten E.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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>MEDLINE - Academic</collection><jtitle>Blood</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>To, L. Bik</au><au>Levesque, Jean-Pierre</au><au>Herbert, Kirsten E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>How I treat patients who mobilize hematopoietic stem cells poorly</atitle><jtitle>Blood</jtitle><addtitle>Blood</addtitle><date>2011-10-27</date><risdate>2011</risdate><volume>118</volume><issue>17</issue><spage>4530</spage><epage>4540</epage><pages>4530-4540</pages><issn>0006-4971</issn><eissn>1528-0020</eissn><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-3</notes><notes>content type line 23</notes><notes>ObjectType-Review-1</notes><abstract>Transplantation with 2-5 × 106 mobilized CD34+cells/kg body weight lowers transplantation costs and mortality. Mobilization is most commonly performed with recombinant human G-CSF with or without chemotherapy, but a proportion of patients/donors fail to mobilize sufficient cells. BM disease, prior treatment, and age are factors influencing mobilization, but genetics also contributes. Mobilization may fail because of the changes affecting the HSC/progenitor cell/BM niche integrity and chemotaxis. Poor mobilization affects patient outcome and increases resource use. Until recently increasing G-CSF dose and adding SCF have been used in poor mobilizers with limited success. However, plerixafor through its rapid direct blockage of the CXCR4/CXCL12 chemotaxis pathway and synergy with G-CSF and chemotherapy has become a new and important agent for mobilization. Its efficacy in upfront and failed mobilizers is well established. To maximize HSC harvest in poor mobilizers the clinician needs to optimize current mobilization protocols and to integrate novel agents such as plerixafor. 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| subjects | Anemia, Aplastic Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Biological and medical sciences Bone Marrow Diseases Bone Marrow Failure Disorders Bone marrow, stem cells transplantation. Graft versus host reaction Hematologic and hematopoietic diseases Hematologic Neoplasms - therapy Hematopoietic Stem Cell Mobilization - methods Hematopoietic Stem Cell Transplantation - methods Hematopoietic Stem Cells - pathology Hematopoietic Stem Cells - physiology Hemoglobinuria, Paroxysmal - therapy Humans Medical sciences Models, Biological Transfusions. Complications. Transfusion reactions. Cell and gene therapy Transplantation Conditioning - methods Treatment Failure |
| title | How I treat patients who mobilize hematopoietic stem cells poorly |
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