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Background  Deregulation of the MAPK genes signalling caused by somatic mutations have been implied in leukaemia pathogenesis, including  RAS  mutation ( RAS  mut ) in acute myeloid leukaemia (AML), which has been associated with intra-uterine chemical exposures. A case-case study was conducted in order to explore maternal and child exposures to tobacco smoking associations with early age leukaemia (EAL).    Methods  Covariables of reference were  MLL  rearrangements ( MLL -r),  RAS  mut  and  NQO1  rs1800566 (C609T). Samples from 150 acute lymphoblastic leukaemia (ALL) and 85 AML were included. Maternal exposures were assessed using a structured questionnaire with demographic, personal habits and residence history information. Restriction fragment length polymorphism and denaturing high performance liquid chromatography were used to screen  FLT3, KRAS,  and  NRAS  mutations; direct sequencing was performed to validate the results.  NQO1  polymorphism was detected by real-time allelic discrimination technique.    Results  Overall,  RAS  mut  were detected in 28.7% of EAL cases;  BRAF  mut  was found only in one AML patient. Higher rate of  KRAS  mut  was found in ALL (30.3%) compared to AML (20.8%) with  MLL -r;  RAS  mut  showed an association with second-hand tobacco smoking exposures (OR, 3.06, 95% CI, 1.03-9.07). A considerable increased risk for EAL with the combination of  RAS  mut  and  NQO1  609CT (OR, 4.24, 95% CI, 1.24-14.50) was observed.    Conclusions  Our data demonstrated the increased risk association between maternal smoking and EAL with  MLL -r. Additionally, suggests that children second-hand tobacco exposures are associated with increased risk of EAL with  RAS  mut  modulated by  NQO1  rs1800566 (C609T).

RAS mutations in early age leukaemia modulated by NQO1 rs1800566 (C609T) are associated with second-hand smoking exposures