leukemia/니코틴

Metabolic polymorphisms may influence the risk of childhood leukaemia related to maternal tobacco, coffee or alcohol consumption. The data were extracted from a case-control study including 280 cases of acute leukaemia and 288 controls. Blood sampling was obtained for a representative subset of 219

The association between tobacco smoke and acute myeloid leukemia (AML) is well established in adults but not in children. Individual-level data on parental cigarette smoking were obtained from 12 case-control studies from the Childhood Leukemia International Consortium (CLIC, 1974-2012), including

BACKGROUND Parental smoking and exposure of the mother or the child to environmental tobacco smoke (ETS) as risk factors for Acute non-Lymphocytic Leukemia (AnLL) were investigated. METHODS Incident cases of childhood AnLL were enrolled in 14 Italian Regions during 1998-2001. We estimated odds

We studied the conversion of arachidonic acid or prostaglandin H2 into eicosanoids in promyelocytic leukemia cells (HL-60) that were differentiating into macrophages or neutrophils. Our results indicate that several enzymes of eicosanoid synthesis are coordinately and differentially upregulated

BACKGROUND Cigarette smoking has been associated with acute myeloid leukemia (AML) but hypothesis on the association between maternal smoking during pregnancy and childhood leukemia remains unclear. OBJECTIVE To investigate the association between maternal exposure to tobacco smoking during

BACKGROUND Tobacco smoke contains carcinogens known to damage somatic and germ cells. We investigated the effect of tobacco smoke on the risk of childhood acute lymphoblastic leukemia (ALL) and myeloid leukemia (AML), especially subtypes of prenatal origin such as ALL with translocation t(12;21) or

Tobacco smoke exposure has been associated with risk of childhood acute lymphoblastic leukemia (ALL). Understanding the relationship between tobacco exposures and specific mutations may yield etiologic insights. We carried out a case-only analysis to explore whether prenatal and early-life tobacco

Although some epidemiological studies have published findings supporting the hypothesis that smokers are at a higher risk of developing leukemia, the causal relationship between tobacco and leukemia has not been considered conclusive due to the weak association found, to the lack of a dose-response

BACKGROUND The role of environmental tobacco smoke (ETS) in the causation of lung and breast cancer has been repeatedly evaluated over recent years. In contrast, its impact on the risk of adult leukemia has received little attention. METHODS We used the lifetime residential and occupational ETS

Addition of nicotine causes a dose- and time-dependent inhibition of cell growth in the human promyelocytic HL-60 leukemia cells, with 4 mM nicotine resulting in a 50% inhibition of cellular proliferation after 48-50 h. Accompanying the anticellular effect of nicotine is a significant change in the

Childhood acute lymphoblastic leukemia (ALL) is a biologically heterogeneous disease, and mutations in the KRAS and NRAS oncogenes are present at diagnosis in about one-fifth of cases. Ras mutations were previously associated with environmental exposures in leukemias as well as in many other cancer

OBJECTIVE Tobacco smoke could cause childhood acute lymphoblastic leukemia (ALL) through at least three pathways: (1) prenatal parental smoking; (2) fetal exposure through maternal smoking during pregnancy; and (3) childhood exposure to secondhand smoke (SHS). We tested these hypotheses in a large

In a prospective cohort study of more than 330,000 Swedish construction workers, we explored the effect of tobacco smoking, oral moist snuff use, and body mass index (BMI) on the risk of developing leukemia (excluding chronic lymphocytic leukemia) and multiple myeloma (MM). Study subjects were