Publications by authors named "Bruno Alves de Aguiar Goncalves"
Article Synopsis
- Recent research indicates that early-age acute myeloid leukemia (i-AML) is likely linked to prenatal exposures, particularly to benzene metabolites, affected by genetic factors.
- A study analyzed genetic variations in several genes (CYP2E1, EPHX1, MPO, NQO1, GSTM1, and GSTT1) among 101 i-AML patients and 416 healthy controls to determine their association with i-AML risk.
- The EPHX1 gene variant rs1051740 notably increased i-AML risk, and its diminished enzyme activity may contribute to this vulnerability, highlighting its importance in understanding genetic predispositions to this type of leukemia.
Background: Deregulation of the MAPK genes signalling caused by somatic mutations have been implied in leukaemia pathogenesis, including RAS mutation (RASmut) 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), RASmut and NQO1 rs1800566 (C609T).
NQO1 rs1800566 (C609T), PON1 rs662 (Q192R), and PON1 rs854560 (L55M) polymorphisms segregate the risk of childhood acute leukemias according to age range distribution.
Cancer Causes Control
November 2012
Purpose: The risk of developing childhood leukemia has been associated with gene polymorphisms that decrease the activity of detoxifying metabolic enzymes and enzymes involved in systemic oxidative stress. We investigated the NQO1 and PON1 polymorphisms for associations with susceptibility to childhood leukemia.
Methods: Samples from 1,027 Brazilian children (519 acute lymphoblastic leukemia, ALL; 107 acute myeloid leukemia, AML; 401 controls) were analyzed.
Seven single nucleotide polymorphisms (SNPs) were genotyped in 535 Brazilian children (158 with acute lymphoblastic leukemia [ALL], 74 with acute myeloid leukemia [AML] and 303 controls). The subjects were classified as fast or slow acetylators based on their genotypic variants. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals.
View Article and Find Full Text PDFBackground: Maternal exposure to dipyrone during pregnancy has been associated with risk of infant leukemia (IL). N-Acetyltransferase 2 (NAT2) enzyme acetylates dipyrone, resulting in a detoxified metabolite. We performed genotyping to identify the distribution of NAT2 polymorphisms in duo samples from mothers and children previously investigated in a case-controlled study of IL.
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