Authors’ contributions All named authors conceived the study, participated in its design and coordination and helped to draft the manuscript. All authors read and approved
the final manuscript.”
“Introduction Acute myeloid leukemia (AML), also known as acute nonlymphocytic leukemia (ANLL), is the most common acute leukemia mostly affecting adults, characterized by the rapid growth of abnormal white blood cells in the bone marrow and impaired production of normal blood cells. The mechanisms for AML genesis are still rarely understood. Evidence suggests that radiation, smoking, obesity and exposure to chemical carcinogens are considered as its possible risk factors [1]. Nevertheless, Pifithrin-�� AML only develops in
a small proportion of people exposed to these environmental and lifestyle risk factors, TSA HDAC indicating that the host genetic background might play a critical role in its genesis. Several genetic polymorphisms have been determined as possible risk factors for leukemia by meta-analyses. Variations of GSTM1, GSTT1, MTHFR C677T and XRCC1 Arg399Gln have been indicated to raise leukemia susceptibility [2–4]. Nevertheless, polymorphic MTR A2756G has been shown to decrease acute leukemia risk [5]. Therefore, different genetic polymorphisms might exert different effects on leukemia risk. Nevertheless, only a few gene polymorphisms associated with leukemia susceptibility have been identified to date. Recent evidence indicates that carcinogen-metabolizing genes might play critical roles in determining individual susceptibility to cancers [6]. Susceptibility to cancer is determined by the activation of enzymes involved in carcinogen activation or deactivation. Polymorphisms in these genes encoding the enzymes, possibly by altering their functions, might increase or decrease carcinogen activation/detoxification
and modulate DNA repair process. Cytochrome P450 (CYP) enzymes catalyze Phase I metabolism reaction. Cytochrome P450 1A1 (CYP1A1) is a member of the CYP family that participates in the metabolism of xenobiotics and endogenous compounds, particularly polycyclic aromatic hydrocarbons (PAHs) such as benzo[a]pyrene in smoke [7]. A commonly studied single nucleotide polymorphism (SNP) in the CYP1A1 gene has been indicated to associate with cancer susceptibility. Akt inhibitor The SNP locates at nucleotide 3801 in the 3’ non-coding region containing a single T to C base substitution that results in a polymorphic restriction site for the MspI enzyme (MspI or CYP1A1*2A polymorphism, rs4646903). The MspI restriction site polymorphism results in three genotypes: a predominant homozygous m1 allele without the MspI site (type A, TT), the heterozygote (type B, TC) and a homozygous rare m2 allele with the MspI site (type C, CC) [8]. Published studies devoted to the relationship between CYP1A1 MspI polymorphism and AML risk have generated controversial results.
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