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lung neoplasms/majs
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Inhalation of iron-abundant gas metal arc welding-mild steel fume promotes lung tumors in mice.
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Welding fumes were reclassified as a Group 1 carcinogen by the International Agency for Research on Cancer in 2017. Gas metal arc welding (GMAW) is a process widely used in industry. Fume generated from GMAW-mild steel (MS) is abundant in iron with some manganese, while GMAW-stainless steel (SS)
Lung tumor promotion by chromium-containing welding particulate matter in a mouse model.
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BACKGROUND
Epidemiology suggests that occupational exposure to welding particulate matter (PM) may increase lung cancer risk. However, animal studies are lacking to conclusively link welding with an increased risk. PM derived from stainless steel (SS) welding contains carcinogenic metals such as
Chemotherapeutic efficacy of paclitaxel in combination with Withania somnifera on benzo(a)pyrene-induced experimental lung cancer.
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Lung cancer is one of the leading causes of cancer death in the world and is notoriously difficult to treat effectively. In the present study, male Swiss albino mice were divided into five groups of six animals each: group I animals received corn oil orally and served as a control; group II
Increased expression of cyclooxygenase-2 in rat lung tumors induced by the tobacco-specific nitrosamine 4-(methylnitrosamino)-4-(3-pyridyl)-1-butanone: the impact of a high-fat diet.
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Aberrant or excessive expression of cyclooxygenase (COX)-2 has been implicated in the pathogenesis of many disease processes, including carcinogenesis. COX-2 expression was immunohistochemically examined in archival samples (D. Hoffmann et al., Cancer Res., 53: 2758-2761, 1993) of lung neoplasms
[Experimental study on lung neoplasm model induced by 3, 4-benzopyrene pulmonary injection in rats].
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BACKGROUND
There is still disadvantage in animal model for lung cancer study, no matter what is xenograft nude mice or rats/mice lung neoplasm induced by carcinogenesis.The purpose of the current investigation is to explore a simple and convenient and reliable method for lung neoplasm animal
Melanoma lung metastases and cytolytic effector cells in mice fed antioxidant-balanced corn oil or fish oil diets.
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(C57BL/6 x DBA/2)F1 mice were fed antioxidant-matched fish oil (FO) or corn oil (CO) diets for weeks, were challenged with B16.F10 melanoma cells, and lung metastases were enumerated 17 days later. Mice fed FO had fewer lung tumors than mice fed CO. This dietary effect persisted in mice injected
Effects of alkyl chain length on the inhibition of NNK-induced lung neoplasia in A/J mice by arylalkyl isothiocyanates.
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Six homologous arylakyl isothiocyanates were evaluated for their abilities to inhibit pulmonary adenomas induced by the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in A/J mice. Four consecutive daily doses (5 mumol/mouse) of phenyl isothiocyanate (PITC), benzyl
4-(Methylnitrosamino)-I-(3-pyridyl)-1-butanone enhances the expression of apolipoprotein A-I and Clara cell 17-kDa protein in the lung proteomes of rats fed a corn oil diet but not a fish oil diet.
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The nicotine-derived nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is one of the most potent lung carcinogens in rodents. Several epidemiologic studies indicated that the development of lung cancer in smokers is influenced by the type and amount of dietary polyunsaturated fatty
[Prevention of chinese green tea on 3,4-benzopyrene-induced lung cancer and its mechanism in animal mode.].
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BACKGROUND
Chinese green tea is one of the daily consumption beverages in the world and is considered a promising cancer chemopreventive agent. In the present study, we investigate the role of lung cancer prevention by green tea and its mechanism.
METHODS
Three groups of female SD rats were kept
The effects of phenethyl isothiocyanate, N-acetylcysteine and green tea on tobacco smoke-induced lung tumors in strain A/J mice.
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Male and female strain A/J mice were exposed to a mixture of cigarette sidestream and mainstream smoke at a chamber concentration of total suspended particulates of 82.5 mg/m3. Exposure time was 6 h/day, 5 days/week for 5 months. The animals were allowed to recover for another 4 months in filtered
Beta-carotene and lung cancer in smokers: review of hypotheses and status of research.
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A number of epidemiological studies have reported associations of beta-carotene plasma levels or intake with decreased lung cancer risk. However, intervention studies in smokers have unexpectedly reported increased lung tumor rates after high, long-term, beta-carotene supplementation. Recently,
CYP1B1 determines susceptibility to low doses of 7,12-dimethylbenz[a]anthracene-induced ovarian cancers in mice: correlation of CYP1B1-mediated DNA adducts with carcinogenicity.
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We showed previously that CYP1B1-null mice developed 10 times less lymphomas than wild-type mice after receiving 7,12-dimethylbenz[a]anthracene (DMBA). In this study a 10-fold lower dose was applied to differentiate between toxicity induced lymphomas (200 micro g/mouse/day) and tumor initiation (20
Strain comparison of systemic N-nitrosohexamethyleneimine carcinogenesis in BALB/c, SENCAR and CD-1 mice.
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SENCAR mice have been selectively bred for hypersusceptibility to 2-stage chemical skin carcinogenesis. In this study the relative susceptibilities of SENCAR, BALB/c and CD-1 mice to systemic carcinogenesis by N-nitrosohexamethyleneimine (NHEX) were examined. NHEX was administered twice weekly (1
Tumorigenesis of 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), but not enhancing effects of concomitant high-fat diet, on lung carcinogenesis in female A/J mice.
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It has been reported that 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) induces liver tumors and to a lesser extent lung lesions, lymphomas and leukemias in CDF(1) mice. Since a number of case control studies have pointed to a positive association between fat consumption and lung cancer, we
Vanadium pentoxide induces pulmonary inflammation and tumor promotion in a strain-dependent manner.
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BACKGROUND
Elevated levels of air pollution are associated with increased risk of lung cancer. Particulate matter (PM) contains transition metals that may potentiate neoplastic development through the induction of oxidative stress and inflammation, a lung cancer risk factor. Vanadium pentoxide
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