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您的检索式：作者名="CASTO Bruce C"
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| 1 | Cyclooxygenase-2 and the inflammogenesis of breast cancer显示文摘Cohesive scientific evidence from molecular, animal, and human investigations supports the hypothesis that constitutive overexpression of cyclooxygenase-2(COX-2) is a ubiquitous driver of mammary carcinogenesis, and reciprocally, that COX-2 blockade has strong potential for breast cancer prevention and therapy. Key findings include the following:(1) COX-2 is constitutively expressed throughout breast cancer development and expression intensifies with stage at detection, cancer progression and metastasis;(2) essential features of mammary carcinogenesis(mutagenesis, mitogenesis, angiogenesis, reduced apoptosis, metastasis and immunosuppression) are linked to COX-2-driven prostaglandin E2(PGE-2) biosynthesis;(3) upregulation of COX-2 and PGE-2 expression induces transcription of CYP-19 and aromatase-catalyzed estrogen biosynthesis which stimulates unbridled mitogenesis;(4) extrahe-patic CYP-1B1 in mammary adipose tissue converts paracrine estrogen to carcinogenic quinones with mutagenic impact; and(5) agents that inhibit COX-2 reduce the risk of breast cancer in women without disease and reduce recurrence risk and mortality in women with breast cancer. Recent sharp increases in global breast cancer incidence and mortality are likely driven by chronic inflammation of mammary adipose and upregulation of COX-2 associated with the obesity pandemic. The totality of evidence clearly supports the supposition that mammary carcinogenesis often evolves as a progressive series of highly specific cellular and molecular changes in response to induction of constitutive overexpression of COX-2 and the prostaglandin cascade in the 'inflammogenesis of breast cancer'. | Randall E Harris Bruce C Casto Zachary M Harris | 2014 | World Journal of Clinical Oncology2014，5，4： | 15 |
| 2 | Nicotine-induced upregulation of antioxidant protein Prx 1 in oral squamous cell carcinoma显示文摘Nicotine is a source of exogenous oxidative stress, which is associated with the pathogenesis of numerous diseases including oral squamous cell carcinoma (OSCC), whereas an antioxidant protein, peroxiredoxin 1 (Prx 1), plays an important role in the modulation of this condition. This study was to investigate the association between Prx 1 and tobacco-induced oxidative stress. The expression of Prx 1 and GST in OSCC Tca8113 cells, which were pre-treated with nicotine, was determined. In the present study, MTT assay, reactive oxygen species (ROS) assay, RT-PCR and Western blot analyses, respectively, were conducted to assess cell viability, ROS level, and expression level of Prx 1 and GST in nicotine-treated Tca8113 cells. Nuclear factor kappa B (NF- B) expression was detected by immuno-fluorescence. Our results showed the growth of Tca8113 cells was increased in a dose-dependent manner when cells were treated with nicotine at concentrations from 0.1 to 10 mol/L, but the proliferation of the cells decreased at 100 mol/L. ROS levels increased in all groups treated with nicotine at concentrations of 0.1, 1, 10, or 100 mol/L for 24h. Prx 1 and GST mRNA and protein expression were up-regulated in cells treated with nicotine for the same time at different concentrations or at the same concentration for different times (P<0.05). NF-B was translocated from cytoplasm to nucleus, the expression of NF- B was increased in nucleus. These results suggest that up-regulation of Prx1 expression appears to be associated with tobacco-induced oxidative stress, which may play an important role in the pathogenesis of OSCC. | ZHAO YanHua ZHANG Min YAN Fei CASTO Bruce C TANG XiaoFei | 2013 | Chinese Science Bulletin2013，58，16： | 7 |
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