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Study Links Malaria to Childhood Cancer Through Immune System Enzyme

New research identifies sustained AID activity in malaria-infected children as a driver of MYC translocations leading to Burkitt lymphoma.

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Overview

  • Groundbreaking research reveals how Plasmodium falciparum malaria infection triggers sustained activation-induced cytidine deaminase (AID) activity in B cells, leading to oncogenic MYC translocations.
  • Burkitt lymphoma, a highly aggressive childhood cancer, is ten times more prevalent in regions with persistent P. falciparum transmission, such as equatorial Africa and New Guinea.
  • The study confirms elevated and functional AID levels in B cells of children with uncomplicated malaria, establishing a direct molecular pathway to lymphoma development.
  • Researchers conducted immunological assays on blood samples from Kenyan children, comparing infected individuals with uninfected controls to validate findings.
  • Experts advocate for malaria control strategies, including vector management and vaccination, to reduce both malaria transmission and associated cancer risk in endemic regions.