adenocarcinoma/nicotina

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Induction of monocyte chemoattractant protein-1 by nicotine in pancreatic ductal adenocarcinoma cells: role of osteopontin.

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BACKGROUND Cigarette smoke and nicotine are among the leading environmental risk factors for developing pancreatic ductal adenocarcinoma (PDA). We showed recently that nicotine induces osteopontin (OPN), a protein that plays critical roles in inflammation and tumor metastasis. We identified an OPN

Role of nicotine dependence on the relationship between variants in the nicotinic receptor genes and risk of lung adenocarcinoma.

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Several variations in the nicotinic receptor genes have been identified to be associated with both lung cancer risk and smoking in the genome-wide association (GWA) studies. However, the relationships among these three factors (genetic variants, nicotine dependence, and lung cancer) remain unclear.

Relationship between the loss of heterozygosity and tobacco smoking in pulmonary adenocarcinoma.

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A loss of heterozygosity (LOH) is a major cause of lung carcinogenesis, and it is considered to be related to tobacco smoking in central type lung cancer. We investigated the relationship between LOH in lung adenocarcinoma and tobacco smoking. In a consecutive series of 50 patients with lung

Cytotoxic and proliferative effect of tobacco products on Lewis lung adenocarcinoma cells and spleen lymphocytes.

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The effect of tobacco products (TP) on the proliferation of lung adenocarcinoma cells (3LL) and mice spleen lymphocytes as well as on tumor growth and metastasis was analyzed. High concentrations of cigarette smoke condensate (CSC) or tobacco extract (TE) were cytotoxic for tumoral and lymphoid

The biological significance of tobacco-specific N-nitrosamines: smoking and adenocarcinoma of the lung.

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In the U.S., there has been a steeper rise of the incidence of lung adenocarcinoma than of squamous cell carcinoma of the lung among cigarette smokers. Since 1950, the percentage of all cigarettes sold that had filter tips increased from 0.56 to 92% in 1980 and to 97% in 1990. The tobacco of the

Gene-expression profiles in lung adenocarcinomas related to chronic wood smoke or tobacco exposure.

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BACKGROUND Tobacco-smoke is the major etiological factor related to lung cancer. However, other important factor is chronic wood smoke exposure (WSE). Approximately 30 % of lung cancer patients in Mexico have a history of WSE, and present different clinical, pathological and molecular

Comparative functional genomics analysis of NNK tobacco-carcinogen induced lung adenocarcinoma development in Gprc5a-knockout mice.

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BACKGROUND Improved understanding of lung cancer development and progression, including insights from studies of animal models, are needed to combat this fatal disease. Previously, we found that mice with a knockout (KO) of G-protein coupled receptor 5A (Gprc5a) develop lung tumors after a long

Association of adenocarcinoma and squamous cell carcinoma of the esophagus with tobacco-related and other malignancies.

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Little is known about the etiology of esophageal and gastric cardia adenocarcinoma (EGA), a cancer with one of the fastest-rising incidences in the developed world. To explore the etiology of this cancer, we conducted a retrospective cohort analysis using data from the Surveillance, Epidemiology and

Exposure to environmental tobacco smoke and risk of adenocarcinoma of the lung.

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We conducted a case-control study of adenocarcinoma of the lung and exposure to environmental tobacco smoke (ETS) in 7 countries. We interviewed 70 cases of adenocarcinoma of the lung and 178 population or hospital controls. All subjects had smoked fewer than 400 cigarettes in their lifetimes. Ever

snoRNA and piRNA expression levels modified by tobacco use in women with lung adenocarcinoma.

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Lung cancer is one of the most frequent types of cancer worldwide. Most patients are diagnosed at advanced stage and thus have poor prognosis. Smoking is a risk factor for lung cancer, however most smokers do not develop lung cancer while 20% of women with lung adenocarcinoma are non-smokers.

Laser capture microdissection and microarray expression analysis of lung adenocarcinoma reveals tobacco smoking- and prognosis-related molecular profiles.

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Recent expression profile analyses revealed that lung adenocarcinomas can be divided into several subgroups with diverse pathological features. Because cellular heterogeneity of tumors can confound these analyses, we used laser capture microdissection and microarray expression analysis to

Combinations of N-Acetyl-S-(N-2-Phenethylthiocarbamoyl)-L-Cysteine and myo-inositol inhibit tobacco carcinogen-induced lung adenocarcinoma in mice.

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We have previously generated convincing evidence that combinations of N-acetyl-S-(N-2-phenethylthiocarbamoyl)-L-cysteine (PEITC-NAC; 3 micromol/g diet) and myo-inositol (MI; 56 micromol/g diet) were significantly more effective than the individual compounds as inhibitors of tobacco smoke

Adenocarcinoma of the esophagus and esophagogastric junction in white men in the United States: alcohol, tobacco, and socioeconomic factors.

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In the United States, the incidence of adenocarcinoma of the esophagus, including the esophagogastric (EG) junction, has been increasing rapidly over the past two decades. Except for an association with Barrett's esophagus, little is known about the etiology of these cancers. A population-based

Tobacco chemical-induced mouse lung adenocarcinoma cell lines pin the prolactin orthologue proliferin as a lung tumour promoter.

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Lung adenocarcinoma (LADC) is the leading cause of cancer death worldwide. Nevertheless, syngeneic mouse models of the disease are sparse, and cell lines suitable for transplantable and immunocompetent mouse models of LADC remain unmet needs. We established multiple mouse LADC cell lines by

Adenocarcinomas of the esophagus and gastric cardia: medical conditions, tobacco, alcohol, and socioeconomic factors.

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Adenocarcinomas of the esophagus and gastric cardia have increased in incidence over the past 10-15 years in Western countries. The cause for this increase in incidence is still unknown. Our study was designed to investigate potential risk factors for adenocarcinomas of the esophagus and gastric

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