HLA-DP genetic variation, proxies for early life immune modulation and childhood acute lymphoblastic leukemia risk
The human leukocyte antigen (HLA) genes are candidate genetic susceptibility loci for childhood acute lymphoblastic leukemia (ALL). We examined the effect of HLA-DP genetic variation on risk and evaluated its potential interaction with 4 proxies for early immune modulation, including measures of inf...
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| Veröffentlicht in: | Blood 2012-10, Vol.120 (15), p.3039-3047 |
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| creator | Urayama, Kevin Y. Chokkalingam, Anand P. Metayer, Catherine Ma, Xiaomei Selvin, Steve Barcellos, Lisa F. Wiemels, Joseph L. Wiencke, John K. Taylor, Malcolm Brennan, Paul Dahl, Gary V. Moonsamy, Priscilla Erlich, Henry A. Trachtenberg, Elizabeth Buffler, Patricia A. |
| description | The human leukocyte antigen (HLA) genes are candidate genetic susceptibility loci for childhood acute lymphoblastic leukemia (ALL). We examined the effect of HLA-DP genetic variation on risk and evaluated its potential interaction with 4 proxies for early immune modulation, including measures of infectious exposures in infancy (presence of older siblings, daycare attendance, ear infections) and breastfeeding. A total of 585 ALL cases and 848 controls were genotyped at the HLA-DPA1 and DPB1 loci. Because of potential heterogeneity in effect by race/ethnicity, we included only non-Hispanic white (47%) and Hispanic (53%) children and considered these 2 groups separately in the analysis. Logistic regression analyses showed an increased risk of ALL associated with HLA-DPB1*01:01 (odds ratio [OR] = 1.43, 95% CI, 1.01-2.04) with no heterogeneity by Hispanic ethnicity (P = .969). Analyses of DPB1 supertypes showed a marked childhood ALL association with DP1, particularly for high-hyperdiploid ALL (OR = 1.83; 95% CI, 1.20-2.78). Evidence of interaction was found between DP1 and older sibling (P = .036), and between DP1 and breastfeeding (P = .094), with both showing statistically significant DP1 associations within the lower exposure categories only. These findings support an immune mechanism in the etiology of childhood ALL involving the HLA-DPB1 gene in the context of an insufficiently modulated immune system. |
| doi_str_mv | 10.1182/blood-2012-01-404723 |
| format | Article |
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We examined the effect of HLA-DP genetic variation on risk and evaluated its potential interaction with 4 proxies for early immune modulation, including measures of infectious exposures in infancy (presence of older siblings, daycare attendance, ear infections) and breastfeeding. A total of 585 ALL cases and 848 controls were genotyped at the HLA-DPA1 and DPB1 loci. Because of potential heterogeneity in effect by race/ethnicity, we included only non-Hispanic white (47%) and Hispanic (53%) children and considered these 2 groups separately in the analysis. Logistic regression analyses showed an increased risk of ALL associated with HLA-DPB1*01:01 (odds ratio [OR] = 1.43, 95% CI, 1.01-2.04) with no heterogeneity by Hispanic ethnicity (P = .969). Analyses of DPB1 supertypes showed a marked childhood ALL association with DP1, particularly for high-hyperdiploid ALL (OR = 1.83; 95% CI, 1.20-2.78). Evidence of interaction was found between DP1 and older sibling (P = .036), and between DP1 and breastfeeding (P = .094), with both showing statistically significant DP1 associations within the lower exposure categories only. These findings support an immune mechanism in the etiology of childhood ALL involving the HLA-DPB1 gene in the context of an insufficiently modulated immune system.</description><identifier>ISSN: 0006-4971</identifier><identifier>ISSN: 1528-0020</identifier><identifier>EISSN: 1528-0020</identifier><identifier>DOI: 10.1182/blood-2012-01-404723</identifier><identifier>PMID: 22923493</identifier><language>eng</language><publisher>Washington, DC: Elsevier Inc</publisher><subject>Adolescent ; Adult ; Biological and medical sciences ; Case-Control Studies ; Child ; Child, Preschool ; European Continental Ancestry Group - genetics ; Female ; Genetic Predisposition to Disease ; Genetic Variation - genetics ; Genotype ; Hematologic and hematopoietic diseases ; Hispanic Americans - genetics ; HLA-DP alpha-Chains - genetics ; HLA-DP beta-Chains - genetics ; Humans ; Immunologic Factors ; Infant ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Lymphoid Neoplasia ; Male ; Medical sciences ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - ethnology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology ; Prognosis ; Risk Factors ; Young Adult</subject><ispartof>Blood, 2012-10, Vol.120 (15), p.3039-3047</ispartof><rights>2012 American Society of Hematology</rights><rights>2015 INIST-CNRS</rights><rights>2012 by The American Society of Hematology 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-f3bb0a263e363f90d17cebd2fd9e8fc706d3695a720c8879ebb5960655103a3e3</citedby><cites>FETCH-LOGICAL-c526t-f3bb0a263e363f90d17cebd2fd9e8fc706d3695a720c8879ebb5960655103a3e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26446817$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22923493$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Urayama, Kevin Y.</creatorcontrib><creatorcontrib>Chokkalingam, Anand P.</creatorcontrib><creatorcontrib>Metayer, Catherine</creatorcontrib><creatorcontrib>Ma, Xiaomei</creatorcontrib><creatorcontrib>Selvin, Steve</creatorcontrib><creatorcontrib>Barcellos, Lisa F.</creatorcontrib><creatorcontrib>Wiemels, Joseph L.</creatorcontrib><creatorcontrib>Wiencke, John K.</creatorcontrib><creatorcontrib>Taylor, Malcolm</creatorcontrib><creatorcontrib>Brennan, Paul</creatorcontrib><creatorcontrib>Dahl, Gary V.</creatorcontrib><creatorcontrib>Moonsamy, Priscilla</creatorcontrib><creatorcontrib>Erlich, Henry A.</creatorcontrib><creatorcontrib>Trachtenberg, Elizabeth</creatorcontrib><creatorcontrib>Buffler, Patricia A.</creatorcontrib><title>HLA-DP genetic variation, proxies for early life immune modulation and childhood acute lymphoblastic leukemia risk</title><title>Blood</title><addtitle>Blood</addtitle><description>The human leukocyte antigen (HLA) genes are candidate genetic susceptibility loci for childhood acute lymphoblastic leukemia (ALL). We examined the effect of HLA-DP genetic variation on risk and evaluated its potential interaction with 4 proxies for early immune modulation, including measures of infectious exposures in infancy (presence of older siblings, daycare attendance, ear infections) and breastfeeding. A total of 585 ALL cases and 848 controls were genotyped at the HLA-DPA1 and DPB1 loci. Because of potential heterogeneity in effect by race/ethnicity, we included only non-Hispanic white (47%) and Hispanic (53%) children and considered these 2 groups separately in the analysis. Logistic regression analyses showed an increased risk of ALL associated with HLA-DPB1*01:01 (odds ratio [OR] = 1.43, 95% CI, 1.01-2.04) with no heterogeneity by Hispanic ethnicity (P = .969). Analyses of DPB1 supertypes showed a marked childhood ALL association with DP1, particularly for high-hyperdiploid ALL (OR = 1.83; 95% CI, 1.20-2.78). Evidence of interaction was found between DP1 and older sibling (P = .036), and between DP1 and breastfeeding (P = .094), with both showing statistically significant DP1 associations within the lower exposure categories only. These findings support an immune mechanism in the etiology of childhood ALL involving the HLA-DPB1 gene in the context of an insufficiently modulated immune system.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>European Continental Ancestry Group - genetics</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic Variation - genetics</subject><subject>Genotype</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hispanic Americans - genetics</subject><subject>HLA-DP alpha-Chains - genetics</subject><subject>HLA-DP beta-Chains - genetics</subject><subject>Humans</subject><subject>Immunologic Factors</subject><subject>Infant</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Lymphoid Neoplasia</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - ethnology</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology</subject><subject>Prognosis</subject><subject>Risk Factors</subject><subject>Young Adult</subject><issn>0006-4971</issn><issn>1528-0020</issn><issn>1528-0020</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAYhC1ERZeFf4CQL0g9kPL6I05yQarKRyutBAc4W479pmvqxIudrNh_T7a7tHApJx_8zHg8Q8grBueM1fxdG2J0BQfGC2CFBFlx8YQsWMnrAoDDU7IAAFXIpmKn5HnOPwCYFLx8Rk45b7iQjViQdLW6KD58pTc44Ogt3Zrkzejj8JZuUvzlMdMuJoomhR0NvkPq-34akPbRTeGOpGZw1K59cOs5ETV2GpGGXb9ZxzaYvHcNON1i7w1NPt--ICedCRlfHs8l-f7p47fLq2L15fP15cWqsCVXY9GJtgXDlUChRNeAY5XF1vHONVh3tgLlhGpKU3GwdV012LZlo0CVJQNhZtWSvD_4bqa2R2dxGJMJepN8b9JOR-P1vzeDX-ubuNVCVqycq1qSs6NBij8nzKPufbYYghkwTlmz-SnFoazU_1HG5sKlUGxG5QG1KeacsLtPxEDvl9V3y-r9shqYPiw7y17__Zt70Z8pZ-DNETDZmtAlM1ifHzglpapZ9VALzt1vPSadrcfBovMJ7ahd9I8n-Q2YmMPI</recordid><startdate>20121011</startdate><enddate>20121011</enddate><creator>Urayama, Kevin Y.</creator><creator>Chokkalingam, Anand P.</creator><creator>Metayer, Catherine</creator><creator>Ma, Xiaomei</creator><creator>Selvin, Steve</creator><creator>Barcellos, Lisa F.</creator><creator>Wiemels, Joseph L.</creator><creator>Wiencke, John K.</creator><creator>Taylor, Malcolm</creator><creator>Brennan, Paul</creator><creator>Dahl, Gary V.</creator><creator>Moonsamy, Priscilla</creator><creator>Erlich, Henry A.</creator><creator>Trachtenberg, Elizabeth</creator><creator>Buffler, Patricia A.</creator><general>Elsevier Inc</general><general>Americain Society of Hematology</general><general>American 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><scope>7T5</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20121011</creationdate><title>HLA-DP genetic variation, proxies for early life immune modulation and childhood acute lymphoblastic leukemia risk</title><author>Urayama, Kevin Y. ; Chokkalingam, Anand P. ; Metayer, Catherine ; Ma, Xiaomei ; Selvin, Steve ; Barcellos, Lisa F. ; Wiemels, Joseph L. ; Wiencke, John K. ; Taylor, Malcolm ; Brennan, Paul ; Dahl, Gary V. ; Moonsamy, Priscilla ; Erlich, Henry A. ; Trachtenberg, Elizabeth ; Buffler, Patricia A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-f3bb0a263e363f90d17cebd2fd9e8fc706d3695a720c8879ebb5960655103a3e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>European Continental Ancestry Group - genetics</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetic Variation - genetics</topic><topic>Genotype</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hispanic Americans - genetics</topic><topic>HLA-DP alpha-Chains - genetics</topic><topic>HLA-DP beta-Chains - genetics</topic><topic>Humans</topic><topic>Immunologic Factors</topic><topic>Infant</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Lymphoid Neoplasia</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - ethnology</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology</topic><topic>Prognosis</topic><topic>Risk Factors</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Urayama, Kevin Y.</creatorcontrib><creatorcontrib>Chokkalingam, Anand P.</creatorcontrib><creatorcontrib>Metayer, Catherine</creatorcontrib><creatorcontrib>Ma, Xiaomei</creatorcontrib><creatorcontrib>Selvin, Steve</creatorcontrib><creatorcontrib>Barcellos, Lisa F.</creatorcontrib><creatorcontrib>Wiemels, Joseph L.</creatorcontrib><creatorcontrib>Wiencke, John K.</creatorcontrib><creatorcontrib>Taylor, Malcolm</creatorcontrib><creatorcontrib>Brennan, Paul</creatorcontrib><creatorcontrib>Dahl, Gary V.</creatorcontrib><creatorcontrib>Moonsamy, Priscilla</creatorcontrib><creatorcontrib>Erlich, Henry A.</creatorcontrib><creatorcontrib>Trachtenberg, Elizabeth</creatorcontrib><creatorcontrib>Buffler, Patricia A.</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><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Blood</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Urayama, Kevin Y.</au><au>Chokkalingam, Anand P.</au><au>Metayer, Catherine</au><au>Ma, Xiaomei</au><au>Selvin, Steve</au><au>Barcellos, Lisa F.</au><au>Wiemels, Joseph L.</au><au>Wiencke, John K.</au><au>Taylor, Malcolm</au><au>Brennan, Paul</au><au>Dahl, Gary V.</au><au>Moonsamy, Priscilla</au><au>Erlich, Henry A.</au><au>Trachtenberg, Elizabeth</au><au>Buffler, Patricia A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HLA-DP genetic variation, proxies for early life immune modulation and childhood acute lymphoblastic leukemia risk</atitle><jtitle>Blood</jtitle><addtitle>Blood</addtitle><date>2012-10-11</date><risdate>2012</risdate><volume>120</volume><issue>15</issue><spage>3039</spage><epage>3047</epage><pages>3039-3047</pages><issn>0006-4971</issn><issn>1528-0020</issn><eissn>1528-0020</eissn><abstract>The human leukocyte antigen (HLA) genes are candidate genetic susceptibility loci for childhood acute lymphoblastic leukemia (ALL). We examined the effect of HLA-DP genetic variation on risk and evaluated its potential interaction with 4 proxies for early immune modulation, including measures of infectious exposures in infancy (presence of older siblings, daycare attendance, ear infections) and breastfeeding. A total of 585 ALL cases and 848 controls were genotyped at the HLA-DPA1 and DPB1 loci. Because of potential heterogeneity in effect by race/ethnicity, we included only non-Hispanic white (47%) and Hispanic (53%) children and considered these 2 groups separately in the analysis. Logistic regression analyses showed an increased risk of ALL associated with HLA-DPB1*01:01 (odds ratio [OR] = 1.43, 95% CI, 1.01-2.04) with no heterogeneity by Hispanic ethnicity (P = .969). Analyses of DPB1 supertypes showed a marked childhood ALL association with DP1, particularly for high-hyperdiploid ALL (OR = 1.83; 95% CI, 1.20-2.78). Evidence of interaction was found between DP1 and older sibling (P = .036), and between DP1 and breastfeeding (P = .094), with both showing statistically significant DP1 associations within the lower exposure categories only. These findings support an immune mechanism in the etiology of childhood ALL involving the HLA-DPB1 gene in the context of an insufficiently modulated immune system.</abstract><cop>Washington, DC</cop><pub>Elsevier Inc</pub><pmid>22923493</pmid><doi>10.1182/blood-2012-01-404723</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adolescent Adult Biological and medical sciences Case-Control Studies Child Child, Preschool European Continental Ancestry Group - genetics Female Genetic Predisposition to Disease Genetic Variation - genetics Genotype Hematologic and hematopoietic diseases Hispanic Americans - genetics HLA-DP alpha-Chains - genetics HLA-DP beta-Chains - genetics Humans Immunologic Factors Infant Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Lymphoid Neoplasia Male Medical sciences Precursor Cell Lymphoblastic Leukemia-Lymphoma - ethnology Precursor Cell Lymphoblastic Leukemia-Lymphoma - etiology Prognosis Risk Factors Young Adult |
| title | HLA-DP genetic variation, proxies for early life immune modulation and childhood acute lymphoblastic leukemia risk |
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