{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Broen K"],"funding":["University of Michigan","Simons Foundation","HHS | NIH | NCI | Division of Cancer Epidemiology and Genetics, National Cancer Institute (DCEG)","University of Michigan (UM)","Simons Foundation (SF)","HHS | NIH | NCI | Division of Cancer Epidemiology and Genetics, National Cancer Institute"],"pagination":["e2211055120"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9926229"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["120(2)"],"pubmed_abstract":["Endemic Burkitt lymphoma (eBL) is a pediatric cancer coendemic with malaria in sub-Saharan Africa, suggesting an etiological link between them. However, previous cross-sectional studies of limited geographic areas have not found a convincing association. We used spatially detailed data from the Epidemiology of Burkitt Lymphoma in East African Children and Minors (EMBLEM) study to assess this relationship. EMBLEM is a case-control study of eBL from 2010 through 2016 in six regions of Kenya, Uganda, and Tanzania. To measure the intensity of exposure to the malaria parasite, <i>Plasmodium falciparum</i>, among children in these regions, we used high-resolution spatial data from the Malaria Atlas Project to estimate the annual number of <i>P. falciparum</i> infections from 2000 through 2016 for each of 49 districts within the study region. Cumulative <i>P. falciparum</i> exposure, calculated as the sum of annual infections by birth cohort, varied widely, with a median of 47 estimated infections per child by age 10, ranging from 4 to 315 infections. eBL incidence increased 39% for each 100 additional lifetime <i>P. falciparum</i> infections (95% CI: 6.10 to 81.04%) with the risk peaking among children aged 5 to 11 and declining thereafter. Alternative models using estimated annual <i>P. falciparum</i> infections 0 to 10 y before eBL onset were inconclusive, suggesting that eBL risk is a function of cumulative rather than recent cross-sectional exposure. Our findings provide population-level evidence that eBL is a phenotype related to heavy lifetime exposure to <i>P. falciparum</i> malaria and support emphasizing the link between malaria and eBL."],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Burkitt lymphoma risk shows geographic and temporal associations with <i>Plasmodium falciparum</i> infections in Uganda, Tanzania, and Kenya."],"pmcid":["PMC9926229"],"funding_grant_id":["HHSN261201100063C; HHSN261201100007I","5 T42 OH 8455-15","812255"],"pubmed_authors":["Masalu N","Buller ID","Goedert JJ","Reynolds SJ","Kinyera T","Dickens J","Wekesa WN","Zelner J","Wilson ML","Ayers LW","Otim I","Biggar RJ","Mbulaiteye SM","Legason ID","Nabalende H","Bhatia K","Kuremu RT","Tenge CN","Trangucci R","Kerchan P","Broen K","Ogwang MD","Were PA","Kawira E"],"additional_accession":[]},"is_claimable":false,"name":"Burkitt lymphoma risk shows geographic and temporal associations with <i>Plasmodium falciparum</i> infections in Uganda, Tanzania, and Kenya.","description":"Endemic Burkitt lymphoma (eBL) is a pediatric cancer coendemic with malaria in sub-Saharan Africa, suggesting an etiological link between them. However, previous cross-sectional studies of limited geographic areas have not found a convincing association. We used spatially detailed data from the Epidemiology of Burkitt Lymphoma in East African Children and Minors (EMBLEM) study to assess this relationship. EMBLEM is a case-control study of eBL from 2010 through 2016 in six regions of Kenya, Uganda, and Tanzania. To measure the intensity of exposure to the malaria parasite, <i>Plasmodium falciparum</i>, among children in these regions, we used high-resolution spatial data from the Malaria Atlas Project to estimate the annual number of <i>P. falciparum</i> infections from 2000 through 2016 for each of 49 districts within the study region. Cumulative <i>P. falciparum</i> exposure, calculated as the sum of annual infections by birth cohort, varied widely, with a median of 47 estimated infections per child by age 10, ranging from 4 to 315 infections. eBL incidence increased 39% for each 100 additional lifetime <i>P. falciparum</i> infections (95% CI: 6.10 to 81.04%) with the risk peaking among children aged 5 to 11 and declining thereafter. Alternative models using estimated annual <i>P. falciparum</i> infections 0 to 10 y before eBL onset were inconclusive, suggesting that eBL risk is a function of cumulative rather than recent cross-sectional exposure. Our findings provide population-level evidence that eBL is a phenotype related to heavy lifetime exposure to <i>P. falciparum</i> malaria and support emphasizing the link between malaria and eBL.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2025-04-04T12:41:39.51Z","creation":"2025-04-04T12:41:39.51Z"},"accession":"S-EPMC9926229","cross_references":{"pubmed":["36595676"],"doi":["10.1073/pnas.2211055120"]}}