Vittoria Colamesta1, Silvia D'Aguanno1, Massimo Breccia2, Sara Bruffa1, Claudio Cartoni2, Giuseppe La Torre3. 1. Department of Public Health and Infectious Diseases, "Sapienza"-University of Rome, Italy. 2. Department of Cellular Biotechnologies and Hematology, "Sapienza"-University of Rome, Italy. 3. Department of Public Health and Infectious Diseases, "Sapienza"-University of Rome, Italy. Electronic address: giuseppe.latorre@uniroma1.it.
Abstract
BACKGROUND: The aim was to perform a systematic review and meta-analysis on the relationship between tobacco smoking and the onset of acute myeloid leukemia (AML) in adults. METHODS: PubMed and Scopus databases were systematically searched. In the meta-analysis, random or fixed effects models were used according to the presence of heterogeneity. Study quality was assessed using the Newcastle-Ottawa Scale. RESULTS: Twenty-seven articles were included. Case-control and cohort meta-analyses show that current, ever and former smokers have a significant increased risk to develop AML compared to never smokers [current: OR=1.36 (1.11-1.66) and RR=1.52 (1.10-2.14); ever: OR=1.25 (1.14-1.38) and RR=1.45 (1.10-1.90); former: OR=1.21 (1.03-1.41) and RR=1.45 (1.08-1.94)]. Moreover, increasing smoking intensity and duration is associated with an increase of the risk, OR shift from 1.14 (1-20 pack/years) to 2.36 (>40 pack/years). DISCUSSION AND CONCLUSION: Smoking may have a significant role in AML onset in a multistep pathogenesis.
BACKGROUND: The aim was to perform a systematic review and meta-analysis on the relationship between tobacco smoking and the onset of acute myeloid leukemia (AML) in adults. METHODS: PubMed and Scopus databases were systematically searched. In the meta-analysis, random or fixed effects models were used according to the presence of heterogeneity. Study quality was assessed using the Newcastle-Ottawa Scale. RESULTS: Twenty-seven articles were included. Case-control and cohort meta-analyses show that current, ever and former smokers have a significant increased risk to develop AML compared to never smokers [current: OR=1.36 (1.11-1.66) and RR=1.52 (1.10-2.14); ever: OR=1.25 (1.14-1.38) and RR=1.45 (1.10-1.90); former: OR=1.21 (1.03-1.41) and RR=1.45 (1.08-1.94)]. Moreover, increasing smoking intensity and duration is associated with an increase of the risk, OR shift from 1.14 (1-20 pack/years) to 2.36 (>40 pack/years). DISCUSSION AND CONCLUSION: Smoking may have a significant role in AML onset in a multistep pathogenesis.
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