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telangiectasis/nikotin
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Ataxia-telangiectasia mutated expression is associated with tobacco smoke exposure in esophageal cancer tissues and benzo[a]pyrene diol epoxide in cell lines.
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Esophageal cancer is a substantial health problem because of its usually late stage at diagnosis and poor prognosis. Tobacco smoking and alcohol use are the most important risk factors in the development of esophageal squamous cell carcinoma (SCC). Our previous study demonstrated the binding of
ATM activation accompanies histone H2AX phosphorylation in A549 cells upon exposure to tobacco smoke.
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BACKGROUND
In response to DNA damage or structural alterations of chromatin, histone H2AX may be phosphorylated on Ser139 by phosphoinositide 3-kinase related protein kinases (PIKKs) such as ataxia telangiectasia mutated (ATM), ATM-and Rad-3 related (ATR) kinase, or by DNA dependent protein kinase
Differential responses to high- and low-dose ultraviolet-B stress in tobacco Bright Yellow-2 cells.
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Ultraviolet (UV)-B irradiation leads to DNA damage, cell cycle arrest, growth inhibition, and cell death. To evaluate the UV-B stress-induced changes in plant cells, we developed a model system based on tobacco Bright Yellow-2 (BY-2) cells. Both low-dose UV-B (low UV-B: 740 J m(-2)) and high-dose
Smoking Significantly Impacts Persistence Rates in Embolized Pulmonary Arteriovenous Malformations in Patients with Hereditary Hemorrhagic Telangiectasia.
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Background Embolization is the standard of care for treatment of pulmonary arteriovenous malformations (PAVMs). Persistence of PAVMs after embolization occurs for undefined reasons but may include inflammation related to smoking in dysregulated angiogenesis. Purpose To determine whether patients
DNA damage response induced by exposure of human lung adenocarcinoma cells to smoke from tobacco- and nicotine-free cigarettes.
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Cigarette smoke (CS) is the major cause of lung cancer and contributes to the development of other malignancies. Attempts have been made to construct reduced toxicity cigarettes, presumed to have diminished genotoxic potential. One such product on the market is the tobacco and nicotine free
DNA repair gene polymorphisms and tobacco smoking in the risk for colorectal adenomas.
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DNA damage is thought to play a critical role in the development of colorectal adenoma. Variation in DNA repair genes may alter their capacity to correct endogenous and exogenous DNA damage. We explored the association between common single-nucleotide polymorphisms (SNPs) in DNA repair genes and
Pulmonary Arteriovenous Malformations Are Associated with Silent Brain Infarcts in Hereditary Hemorrhagic Telangiectasia Patients.
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There is a high prevalence of right-to-left shunting pulmonary arteriovenous malformations (PAVMs), which are stroke risk factors, in hereditary hemorrhagic telangiectasia (HHT) patients. While the prevalence of ischemic complications in HHT patients is known, the prevalence of silent brain infarcts
Gastrointestinal Bleeding in Patients with Hereditary Hemorrhagic Telangiectasia: Risk Factors and Endoscopic Findings.
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Accumulation of DNA damage and reduced levels of nicotine adenine dinucleotide in the brains of Atm-deficient mice.
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Ataxia-telangiectasia (A-T) is a human genetic disorder caused by mutational inactivation of the ATM gene. A-T patients display a pleiotropic phenotype, in which a major neurological feature is progressive ataxia due to degeneration of cerebellar Purkinje and granule neurons. Disruption of the mouse
ATM polymorphisms and risk of lung cancer among never smokers.
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The ataxia-telangiectasia mutated (ATM) gene, an important caretaker of overall genome stability, is thought to play a role in the development of human malignancy. Therefore, we hypothesized that sequence variants in ATM may influence the disposition to lung cancer. In this hospital-based matched
γ-H2AX is a sensitive marker of DNA damage induced by metabolically activated 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone.
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4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a nicotine-derived nitrosamine, is a potent pulmonary carcinogen present in tobacco smoke. DNA adducts induced by metabolically activated NNK cause carcinogenesis; however, the DNA adducts are difficult to detect in cultured cells because of low
Epidemiology of chronic venous insufficiency of the lower limbs in the primary care setting.
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OBJECTIVE
The objective of the study was to describe the general characteristics, risk factors and clinical symptoms of patients seeking medical care at the primary care setting because of chronic venous insufficiency.
METHODS
A total of 606 general practitioners throughout Spain participated in
A parallel study of in vitro sensitivity to benzo[a]pyrene diol epoxide and bleomycin in lung carcinoma cases and controls.
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BACKGROUND
Because only a fraction of smokers develop neoplastic lesions, host factors may affect their susceptibility to the carcinogenic effects of tobacco smoke. Benzo[a]pyrene diol epoxide (BPDE) is the metabolic product of benzo[a]pyrene (B[a]P), a constituent of tobacco smoke. Therefore, BPDE
Analysis of individual molecular events of DNA damage response by flow- and image-assisted cytometry.
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This chapter describes molecular mechanisms of DNA damage response (DDR) and presents flow- and image-assisted cytometric approaches to assess these mechanisms and measure the extent of DDR in individual cells. DNA damage was induced by cell treatment with oxidizing agents, UV light, DNA
Cytometry of ATM activation and histone H2AX phosphorylation to estimate extent of DNA damage induced by exogenous agents.
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This review covers the topic of cytometric assessment of activation of Ataxia telangiectasia mutated (ATM) protein kinase and histone H2AX phosphorylation on Ser139 in response to DNA damage, particularly the damage that involves formation of DNA double-strand breaks. Briefly described are molecular
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