Combined and differential effects of alpha‐thalassemia and HbF‐quantitative trait loci in Senegalese hydroxyurea‐free children with sickle cell anemia
Background Our objective was to investigate the combined and differential effects of alpha‐thalassemia –3.7 kb deletion and HbF‐promoting quantitative trait loci (HbF‐QTL) in Senegalese hydroxyurea (HU)‐free children and young adults with sickle cell anemia (SCA). Procedure Steady‐state biological p...
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| Veröffentlicht in: | Pediatric blood & cancer 2019-10, Vol.66 (10), p.e27934-n/a |
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| creator | Gueye Tall, Fatou Martin, Cyril Ndour, El Hadji Malick Renoux, Céline Ly, Indou Déme Connes, Philippe Gueye, Papa Madieye Diallo, Rokhaya Ndiaye Diagne, Ibrahima Diop, Pape Amadou Cissé, Aynina Lopez Sall, Philomène Joly, Philippe |
| description | Background
Our objective was to investigate the combined and differential effects of alpha‐thalassemia –3.7 kb deletion and HbF‐promoting quantitative trait loci (HbF‐QTL) in Senegalese hydroxyurea (HU)‐free children and young adults with sickle cell anemia (SCA).
Procedure
Steady‐state biological parameters and vaso‐occlusive crises (VOC) requiring emergency admission were recorded over a 2‐year period in 301 children with SCA. The age of the first hospitalized VOC was also recorded. These data were correlated with the alpha‐globin and HbF‐QTL genotypes. For the latter, three different genetic loci were studied (XmnI, rs7482144; BCL11A, rs1427407; and the HBS1L‐MYB region, rs28384513) and a composite score was calculated, ranging from zero (none of these three polymorphisms) to six (all three polymorphisms at the homozygous state).
Results
: A positive clinical impact of the HbF‐QTL score on VOC rate, HbF, leucocytes, and C‐reactive protein levels was observed only for patients without alpha‐thalassemia deletion. Conversely, combination of homozygous –3.7 kb deletion with three to six HbF‐QTL was associated with a higher VOC rate. The age of the first hospitalized VOC was delayed for patients with one or two alpha‐thalassemia deletions and at least two HbF‐QTL.
Conclusion
Alpha‐thalassemia –3.7 kb deletion and HbF‐QTL are modulating factors of SCA clinical severity that interact with each other. They should be studied and interpreted together and not separately, at least in HU‐free children. |
| doi_str_mv | 10.1002/pbc.27934 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_hal_p</sourceid><recordid>TN_cdi_hal_primary_oai_HAL_hal_02459654v1</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2261263343</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3874-8bba909f89e82dd552dbe3b5f6f7b2cf5fcc3d6543272653b8e25e2d683ad1933</originalsourceid><addsrcrecordid>eNp1kUtuFDEQhlsIREJgwQWQJTawmMSPdj-WyYgwkUYiErC2_CjTDu7uie1OmB1H4ACcjpPEnQkTCYmVS6XPX1XpL4rXBB8TjOnJRuljWresfFIcEl7yBcekfrqvcXtQvIjxKqMV5s3z4oARRmlD-GHxezn2yg1gkBwMMs5aCDAkJz2CXOsU0WiR9JtO_vn5K3XSyxihd_KeX6nz3L2eZP6RZHI3gFKQLiE_aofcgD7DAN-khwio25ow_thOAWaTDQBId86bPA7dutSh6PR3n5vgfZbPM14Wz6z0EV49vEfF1_MPX5arxfrTx4vl6XqhWVOXi0Yp2eLWNi001BjOqVHAFLeVrRXVllutmal4yWhNK85UA5QDNVXDpCEtY0fF-503nyc2wfUybMUonVidrsXcw7TkbRbckMy-27GbMF5PEJPoXZx3ziuPUxSUVoRWjJWz9u0_6NU4hSFfkqm6wYwRXj0O12GMMYDdb0CwmOMVOV5xH29m3zwYJ9WD2ZN_88zAyQ64dR62_zeJy7PlTnkHHvKzEw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2278033156</pqid></control><display><type>article</type><title>Combined and differential effects of alpha‐thalassemia and HbF‐quantitative trait loci in Senegalese hydroxyurea‐free children with sickle cell anemia</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Gueye Tall, Fatou ; Martin, Cyril ; Ndour, El Hadji Malick ; Renoux, Céline ; Ly, Indou Déme ; Connes, Philippe ; Gueye, Papa Madieye ; Diallo, Rokhaya Ndiaye ; Diagne, Ibrahima ; Diop, Pape Amadou ; Cissé, Aynina ; Lopez Sall, Philomène ; Joly, Philippe</creator><creatorcontrib>Gueye Tall, Fatou ; Martin, Cyril ; Ndour, El Hadji Malick ; Renoux, Céline ; Ly, Indou Déme ; Connes, Philippe ; Gueye, Papa Madieye ; Diallo, Rokhaya Ndiaye ; Diagne, Ibrahima ; Diop, Pape Amadou ; Cissé, Aynina ; Lopez Sall, Philomène ; Joly, Philippe</creatorcontrib><description>Background
Our objective was to investigate the combined and differential effects of alpha‐thalassemia –3.7 kb deletion and HbF‐promoting quantitative trait loci (HbF‐QTL) in Senegalese hydroxyurea (HU)‐free children and young adults with sickle cell anemia (SCA).
Procedure
Steady‐state biological parameters and vaso‐occlusive crises (VOC) requiring emergency admission were recorded over a 2‐year period in 301 children with SCA. The age of the first hospitalized VOC was also recorded. These data were correlated with the alpha‐globin and HbF‐QTL genotypes. For the latter, three different genetic loci were studied (XmnI, rs7482144; BCL11A, rs1427407; and the HBS1L‐MYB region, rs28384513) and a composite score was calculated, ranging from zero (none of these three polymorphisms) to six (all three polymorphisms at the homozygous state).
Results
: A positive clinical impact of the HbF‐QTL score on VOC rate, HbF, leucocytes, and C‐reactive protein levels was observed only for patients without alpha‐thalassemia deletion. Conversely, combination of homozygous –3.7 kb deletion with three to six HbF‐QTL was associated with a higher VOC rate. The age of the first hospitalized VOC was delayed for patients with one or two alpha‐thalassemia deletions and at least two HbF‐QTL.
Conclusion
Alpha‐thalassemia –3.7 kb deletion and HbF‐QTL are modulating factors of SCA clinical severity that interact with each other. They should be studied and interpreted together and not separately, at least in HU‐free children.</description><identifier>ISSN: 1545-5009</identifier><identifier>EISSN: 1545-5017</identifier><identifier>DOI: 10.1002/pbc.27934</identifier><identifier>PMID: 31322815</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>alpha-Thalassemia - genetics ; alpha‐thalassemia ; Anemia ; Anemia, Sickle Cell - genetics ; Child ; Children ; Clonal deletion ; Cognitive science ; Female ; Fetal Hemoglobin - genetics ; G6PD deficiency ; Gene deletion ; Gene loci ; Gene mapping ; genetic modifiers ; Genotype ; Genotypes ; HbF QTL ; Hematology ; Hemoglobin H - genetics ; Humans ; Hydroxyurea ; Leukocytes ; Male ; Oncology ; Pediatrics ; Quantitative Trait Loci ; Senegal ; Senegal haplotype ; Sickle cell anemia ; Sickle cell disease ; Thalassemia ; VOCs ; Volatile organic compounds ; Young adults</subject><ispartof>Pediatric blood & cancer, 2019-10, Vol.66 (10), p.e27934-n/a</ispartof><rights>2019 Wiley Periodicals, Inc.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3874-8bba909f89e82dd552dbe3b5f6f7b2cf5fcc3d6543272653b8e25e2d683ad1933</citedby><cites>FETCH-LOGICAL-c3874-8bba909f89e82dd552dbe3b5f6f7b2cf5fcc3d6543272653b8e25e2d683ad1933</cites><orcidid>0000-0002-2351-9441 ; 0000-0002-9232-0268 ; 0000-0003-3378-5249</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fpbc.27934$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fpbc.27934$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31322815$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://univ-lyon1.hal.science/hal-02459654$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Gueye Tall, Fatou</creatorcontrib><creatorcontrib>Martin, Cyril</creatorcontrib><creatorcontrib>Ndour, El Hadji Malick</creatorcontrib><creatorcontrib>Renoux, Céline</creatorcontrib><creatorcontrib>Ly, Indou Déme</creatorcontrib><creatorcontrib>Connes, Philippe</creatorcontrib><creatorcontrib>Gueye, Papa Madieye</creatorcontrib><creatorcontrib>Diallo, Rokhaya Ndiaye</creatorcontrib><creatorcontrib>Diagne, Ibrahima</creatorcontrib><creatorcontrib>Diop, Pape Amadou</creatorcontrib><creatorcontrib>Cissé, Aynina</creatorcontrib><creatorcontrib>Lopez Sall, Philomène</creatorcontrib><creatorcontrib>Joly, Philippe</creatorcontrib><title>Combined and differential effects of alpha‐thalassemia and HbF‐quantitative trait loci in Senegalese hydroxyurea‐free children with sickle cell anemia</title><title>Pediatric blood & cancer</title><addtitle>Pediatr Blood Cancer</addtitle><description>Background
Our objective was to investigate the combined and differential effects of alpha‐thalassemia –3.7 kb deletion and HbF‐promoting quantitative trait loci (HbF‐QTL) in Senegalese hydroxyurea (HU)‐free children and young adults with sickle cell anemia (SCA).
Procedure
Steady‐state biological parameters and vaso‐occlusive crises (VOC) requiring emergency admission were recorded over a 2‐year period in 301 children with SCA. The age of the first hospitalized VOC was also recorded. These data were correlated with the alpha‐globin and HbF‐QTL genotypes. For the latter, three different genetic loci were studied (XmnI, rs7482144; BCL11A, rs1427407; and the HBS1L‐MYB region, rs28384513) and a composite score was calculated, ranging from zero (none of these three polymorphisms) to six (all three polymorphisms at the homozygous state).
Results
: A positive clinical impact of the HbF‐QTL score on VOC rate, HbF, leucocytes, and C‐reactive protein levels was observed only for patients without alpha‐thalassemia deletion. Conversely, combination of homozygous –3.7 kb deletion with three to six HbF‐QTL was associated with a higher VOC rate. The age of the first hospitalized VOC was delayed for patients with one or two alpha‐thalassemia deletions and at least two HbF‐QTL.
Conclusion
Alpha‐thalassemia –3.7 kb deletion and HbF‐QTL are modulating factors of SCA clinical severity that interact with each other. They should be studied and interpreted together and not separately, at least in HU‐free children.</description><subject>alpha-Thalassemia - genetics</subject><subject>alpha‐thalassemia</subject><subject>Anemia</subject><subject>Anemia, Sickle Cell - genetics</subject><subject>Child</subject><subject>Children</subject><subject>Clonal deletion</subject><subject>Cognitive science</subject><subject>Female</subject><subject>Fetal Hemoglobin - genetics</subject><subject>G6PD deficiency</subject><subject>Gene deletion</subject><subject>Gene loci</subject><subject>Gene mapping</subject><subject>genetic modifiers</subject><subject>Genotype</subject><subject>Genotypes</subject><subject>HbF QTL</subject><subject>Hematology</subject><subject>Hemoglobin H - genetics</subject><subject>Humans</subject><subject>Hydroxyurea</subject><subject>Leukocytes</subject><subject>Male</subject><subject>Oncology</subject><subject>Pediatrics</subject><subject>Quantitative Trait Loci</subject><subject>Senegal</subject><subject>Senegal haplotype</subject><subject>Sickle cell anemia</subject><subject>Sickle cell disease</subject><subject>Thalassemia</subject><subject>VOCs</subject><subject>Volatile organic compounds</subject><subject>Young adults</subject><issn>1545-5009</issn><issn>1545-5017</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kUtuFDEQhlsIREJgwQWQJTawmMSPdj-WyYgwkUYiErC2_CjTDu7uie1OmB1H4ACcjpPEnQkTCYmVS6XPX1XpL4rXBB8TjOnJRuljWresfFIcEl7yBcekfrqvcXtQvIjxKqMV5s3z4oARRmlD-GHxezn2yg1gkBwMMs5aCDAkJz2CXOsU0WiR9JtO_vn5K3XSyxihd_KeX6nz3L2eZP6RZHI3gFKQLiE_aofcgD7DAN-khwio25ow_thOAWaTDQBId86bPA7dutSh6PR3n5vgfZbPM14Wz6z0EV49vEfF1_MPX5arxfrTx4vl6XqhWVOXi0Yp2eLWNi001BjOqVHAFLeVrRXVllutmal4yWhNK85UA5QDNVXDpCEtY0fF-503nyc2wfUybMUonVidrsXcw7TkbRbckMy-27GbMF5PEJPoXZx3ziuPUxSUVoRWjJWz9u0_6NU4hSFfkqm6wYwRXj0O12GMMYDdb0CwmOMVOV5xH29m3zwYJ9WD2ZN_88zAyQ64dR62_zeJy7PlTnkHHvKzEw</recordid><startdate>201910</startdate><enddate>201910</enddate><creator>Gueye Tall, Fatou</creator><creator>Martin, Cyril</creator><creator>Ndour, El Hadji Malick</creator><creator>Renoux, Céline</creator><creator>Ly, Indou Déme</creator><creator>Connes, Philippe</creator><creator>Gueye, Papa Madieye</creator><creator>Diallo, Rokhaya Ndiaye</creator><creator>Diagne, Ibrahima</creator><creator>Diop, Pape Amadou</creator><creator>Cissé, Aynina</creator><creator>Lopez Sall, Philomène</creator><creator>Joly, Philippe</creator><general>Wiley Subscription Services, Inc</general><general>Wiley</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>7T5</scope><scope>7TK</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-2351-9441</orcidid><orcidid>https://orcid.org/0000-0002-9232-0268</orcidid><orcidid>https://orcid.org/0000-0003-3378-5249</orcidid></search><sort><creationdate>201910</creationdate><title>Combined and differential effects of alpha‐thalassemia and HbF‐quantitative trait loci in Senegalese hydroxyurea‐free children with sickle cell anemia</title><author>Gueye Tall, Fatou ; Martin, Cyril ; Ndour, El Hadji Malick ; Renoux, Céline ; Ly, Indou Déme ; Connes, Philippe ; Gueye, Papa Madieye ; Diallo, Rokhaya Ndiaye ; Diagne, Ibrahima ; Diop, Pape Amadou ; Cissé, Aynina ; Lopez Sall, Philomène ; Joly, Philippe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3874-8bba909f89e82dd552dbe3b5f6f7b2cf5fcc3d6543272653b8e25e2d683ad1933</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>alpha-Thalassemia - genetics</topic><topic>alpha‐thalassemia</topic><topic>Anemia</topic><topic>Anemia, Sickle Cell - genetics</topic><topic>Child</topic><topic>Children</topic><topic>Clonal deletion</topic><topic>Cognitive science</topic><topic>Female</topic><topic>Fetal Hemoglobin - genetics</topic><topic>G6PD deficiency</topic><topic>Gene deletion</topic><topic>Gene loci</topic><topic>Gene mapping</topic><topic>genetic modifiers</topic><topic>Genotype</topic><topic>Genotypes</topic><topic>HbF QTL</topic><topic>Hematology</topic><topic>Hemoglobin H - genetics</topic><topic>Humans</topic><topic>Hydroxyurea</topic><topic>Leukocytes</topic><topic>Male</topic><topic>Oncology</topic><topic>Pediatrics</topic><topic>Quantitative Trait Loci</topic><topic>Senegal</topic><topic>Senegal haplotype</topic><topic>Sickle cell anemia</topic><topic>Sickle cell disease</topic><topic>Thalassemia</topic><topic>VOCs</topic><topic>Volatile organic compounds</topic><topic>Young adults</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gueye Tall, Fatou</creatorcontrib><creatorcontrib>Martin, Cyril</creatorcontrib><creatorcontrib>Ndour, El Hadji Malick</creatorcontrib><creatorcontrib>Renoux, Céline</creatorcontrib><creatorcontrib>Ly, Indou Déme</creatorcontrib><creatorcontrib>Connes, Philippe</creatorcontrib><creatorcontrib>Gueye, Papa Madieye</creatorcontrib><creatorcontrib>Diallo, Rokhaya Ndiaye</creatorcontrib><creatorcontrib>Diagne, Ibrahima</creatorcontrib><creatorcontrib>Diop, Pape Amadou</creatorcontrib><creatorcontrib>Cissé, Aynina</creatorcontrib><creatorcontrib>Lopez Sall, Philomène</creatorcontrib><creatorcontrib>Joly, Philippe</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Pediatric blood & cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gueye Tall, Fatou</au><au>Martin, Cyril</au><au>Ndour, El Hadji Malick</au><au>Renoux, Céline</au><au>Ly, Indou Déme</au><au>Connes, Philippe</au><au>Gueye, Papa Madieye</au><au>Diallo, Rokhaya Ndiaye</au><au>Diagne, Ibrahima</au><au>Diop, Pape Amadou</au><au>Cissé, Aynina</au><au>Lopez Sall, Philomène</au><au>Joly, Philippe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Combined and differential effects of alpha‐thalassemia and HbF‐quantitative trait loci in Senegalese hydroxyurea‐free children with sickle cell anemia</atitle><jtitle>Pediatric blood & cancer</jtitle><addtitle>Pediatr Blood Cancer</addtitle><date>2019-10</date><risdate>2019</risdate><volume>66</volume><issue>10</issue><spage>e27934</spage><epage>n/a</epage><pages>e27934-n/a</pages><issn>1545-5009</issn><eissn>1545-5017</eissn><abstract>Background
Our objective was to investigate the combined and differential effects of alpha‐thalassemia –3.7 kb deletion and HbF‐promoting quantitative trait loci (HbF‐QTL) in Senegalese hydroxyurea (HU)‐free children and young adults with sickle cell anemia (SCA).
Procedure
Steady‐state biological parameters and vaso‐occlusive crises (VOC) requiring emergency admission were recorded over a 2‐year period in 301 children with SCA. The age of the first hospitalized VOC was also recorded. These data were correlated with the alpha‐globin and HbF‐QTL genotypes. For the latter, three different genetic loci were studied (XmnI, rs7482144; BCL11A, rs1427407; and the HBS1L‐MYB region, rs28384513) and a composite score was calculated, ranging from zero (none of these three polymorphisms) to six (all three polymorphisms at the homozygous state).
Results
: A positive clinical impact of the HbF‐QTL score on VOC rate, HbF, leucocytes, and C‐reactive protein levels was observed only for patients without alpha‐thalassemia deletion. Conversely, combination of homozygous –3.7 kb deletion with three to six HbF‐QTL was associated with a higher VOC rate. The age of the first hospitalized VOC was delayed for patients with one or two alpha‐thalassemia deletions and at least two HbF‐QTL.
Conclusion
Alpha‐thalassemia –3.7 kb deletion and HbF‐QTL are modulating factors of SCA clinical severity that interact with each other. They should be studied and interpreted together and not separately, at least in HU‐free children.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>31322815</pmid><doi>10.1002/pbc.27934</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-2351-9441</orcidid><orcidid>https://orcid.org/0000-0002-9232-0268</orcidid><orcidid>https://orcid.org/0000-0003-3378-5249</orcidid></addata></record> |
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| subjects | alpha-Thalassemia - genetics alpha‐thalassemia Anemia Anemia, Sickle Cell - genetics Child Children Clonal deletion Cognitive science Female Fetal Hemoglobin - genetics G6PD deficiency Gene deletion Gene loci Gene mapping genetic modifiers Genotype Genotypes HbF QTL Hematology Hemoglobin H - genetics Humans Hydroxyurea Leukocytes Male Oncology Pediatrics Quantitative Trait Loci Senegal Senegal haplotype Sickle cell anemia Sickle cell disease Thalassemia VOCs Volatile organic compounds Young adults |
| title | Combined and differential effects of alpha‐thalassemia and HbF‐quantitative trait loci in Senegalese hydroxyurea‐free children with sickle cell anemia |
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