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dc.contributor.authorMulama, David H
dc.contributor.authorBailey, Jeffrey A
dc.contributor.authorFoley, Joslyn
dc.contributor.authorChelimo, Kiprotich
dc.contributor.authorOuma, Collins
dc.contributor.authorJura, Walter G
dc.contributor.authorOtieno, Juliana
dc.contributor.authorVulule, John
dc.contributor.authorMoormann, Ann M
dc.date.accessioned2018-01-22T11:48:11Z
dc.date.available2018-01-22T11:48:11Z
dc.date.issued2014-02
dc.identifier.urihttps://repository.maseno.ac.ke/handle/123456789/176
dc.description.abstractEndemic Burkitt lymphoma (eBL) is associated with Epstein–Barr virus (EBV) and Plasmodium falciparum coinfections. Malaria appears to dysregulate immunity that would otherwise control EBV, thereby contributing to eBL etiology. Juxtaposed to human genetic variants associated with protection from malaria, it has been hypothesized that such variants could decrease eBL susceptibility, historically referred to as “the protective hypothesis.” Past studies attempting to link sickle cell trait (HbAS), which is known to be protective against malaria, with protection from eBL were contradictory and underpowered. Therefore, using a case–control study design, we examined HbAS frequency in 306 Kenyan children diagnosed with eBL compared to 537 geographically defined and ethnically matched controls. We found 23.8% HbAS for eBL patients, which was not significantly different …en_US
dc.titleSickle cell trait is not associated with endemic Burkitt lymphoma: An ethnicity and malaria endemicity‐matched case–control study suggests factors controlling EBV...en_US
dc.typeArticleen_US


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