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glioma/− nicotine
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Tobacco smoking and alcohol consumption as risk factors for glioma: a case-control study in Melbourne, Australia.
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OBJECTIVE
To investigate possible associations between tobacco smoking and alcohol consumption and the risk of adult glioma.
METHODS
This was a population based, case-control study. Relative risks (RR) were estimated using logistic regression analysis.
METHODS
Melbourne, Australia.
METHODS
These
Dietary and tobacco risk factors for adult onset glioma in the San Francisco Bay Area (California, USA)
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The roles of diet and tobacco in the etiology of primary brain cancer are controversial. In this report, we compare dietary and cigarette smoking histories among 434 adults newly diagnosed with glioma in the San Francisco Bay Area (California, USA) between 1991 and 1994 with frequency age, gender,
Calcium mobilization during nicotine-induced cell death in human glioma and glioblastoma cell lines.
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Nicotine dose-dependently induced cytotoxicity in human glioma (KG-1-C) and glioblastoma (GBS-1, T98G) cell lines, but could not induce internucleosomal DNA cleavage, in contrast to apoptosing human myelogenous leukemic cell lines. Human glioma/glioblastoma cell lines thus might have a chromatin
Nicotine does not affect stem cell properties requisite for suicide gene therapy against glioma
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Glioblastoma is one of the most lethal tumors in adult central nervous system with a median survival of a year and half and effective therapeutic strategy is urgently needed. For that reason, stem cell-based suicide gene therapies have attracted much interest because of potent tumor tropism of stem
Nicotine enhances proliferation, migration, and radioresistance of human malignant glioma cells through EGFR activation.
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It has been suggested that continued tobacco use during radiation therapy contributes to maintenance of neoplastic growth despite treatment with radiation. Nicotine is a cigarette component that is an established risk factor for many diseases, neoplastic and otherwise. The hypothesis of this work is
Effect of Nicotine on CYP2B1 Expression in a Glioma Animal Model and Analysis of CYP2B6 Expression in Pediatric Gliomas.
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Cyclophosphamide (CPA) is a pro-drug commonly used in the chemotherapeutic schemes for glioma treatment but has high toxicity and the side effects include brain damage and even death. Since CPA is activated mainly by CY2B6, over-expression of the enzyme in the tumor cells has been proposed to
Risk of brain glioma not associated with cigarette smoking or use of other tobacco products in Iowa.
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Nicotine-based surface active ionic liquids: Synthesis, self-assembly and cytotoxicity studies.
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New ester-functionalized surface active ionic liquids (SAILs) based on nicotine, [CnENic][Br] (n=8, 10 and 12), with bromide counterions have been synthesized, characterized and investigated for their self-assembly behavior in aqueous medium. Conductivity measurements in aqueous solutions of the
Nicotine- and tar-free cigarette smoke extract induces cell injury via intracellular Ca2+-dependent subtype-specific protein kinase C activation.
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Nicotine- and tar-free cigarette smoke extract (CSE) is reported to induce cell damage via activation of protein kinase C (PKC) and NADPH oxidase (NOX) in rat C6 glioma cells. Here we determined PKC isozyme(s) activated by CSE and their activation mechanism. In C6 glioma cells, mRNAs for PKCα, PKCδ,
Nicotine- and tar-free cigarette smoke induces cell damage through reactive oxygen species newly generated by PKC-dependent activation of NADPH oxidase.
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We examined cytotoxic effects of nicotine/tar-free cigarette smoke extract (CSE) on C6 glioma cells. The CSE induced plasma membrane damage (determined by lactate dehydrogenase leakage and propidium iodide uptake) and cell apoptosis {determined by MTS
Genetic polymorphisms in glutathione S-transferase mu and theta, N-acetyltransferase, and CYP1A1 and risk of gliomas.
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The role of genetic polymorphisms in modulating susceptibility to carcinogenic exposures has been well explored for tobacco-related neoplasms but not for other neoplasms including gliomas. It is relevant to explore these polymorphisms because certain carcinogenic exposures such as nitrosamines are
Prospective study of cigarette smoking and adult glioma: dosage, duration, and latency.
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Tobacco products are major contributors of exogenous N-nitroso compounds, a group of potent neurocarcinogens. Overall results from studies of smoking and brain tumors have been null, but have provided little information on duration, age at smoking initiation, and latency. We prospectively examined
Cytomegalovirus and glioma: putting the cart before the horse.
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In 1908, Oluf Bang and Vilhelm Ellerman laid the foundation for theory of oncoviruses by demonstrating that the avian erythroblastosis (a form of chicken leukaemia) could be transmitted by cell-free extracts. Since then, it has been shown very convincingly that viruses can directly cause several
Role of IL-8 gene polymorphisms in glioma development in a Chinese population.
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This case-control study aimed to investigate the role of -251 T>A (rs4073) and -781 C>T (rs2227306) polymorphisms in the interleukin-8 (IL-8) gene in the development of glioma in a Chinese population. One hundred and twenty-seven glioma patients and 284 healthy control subjects were recruited to
Endogenous strychnine, nicotine, and morphine--description of hypo and hyper-strychninergic, nicotinergic and morphinergic state in relation to neuropsychiatric diseases.
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Previous work from this laboratory had demonstrated the presence of endogenous morphine, strychnine and nicotine in the mammalian brain and human serum samples. Morphine is synthesised from tyrosine and strychnine and nicotine from tryptophan. This study examines the role of strychnine, nicotine and
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