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  • 1
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2010
    In:  Basic Research in Cardiology Vol. 105, No. 1 ( 2010-1), p. 19-28
    In: Basic Research in Cardiology, Springer Science and Business Media LLC, Vol. 105, No. 1 ( 2010-1), p. 19-28
    Type of Medium: Online Resource
    ISSN: 0300-8428 , 1435-1803
    RVK:
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    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2010
    detail.hit.zdb_id: 1458470-0
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  • 2
    In: JNCI: Journal of the National Cancer Institute, Oxford University Press (OUP), Vol. 104, No. 20 ( 2012-10-17), p. 1599-1611
    Type of Medium: Online Resource
    ISSN: 1460-2105 , 0027-8874
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2012
    detail.hit.zdb_id: 2992-0
    detail.hit.zdb_id: 1465951-7
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  • 3
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 22 ( 2014-11-15), p. 6589-6597
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 22 ( 2014-11-15), p. 6589-6597
    Abstract: Epidemiologic studies linking high serum iron with cancer risks are limited and inconclusive, despite evidence implicating body iron in human carcinogenesis. A cohort of 309,443 adults in Taiwan who had no history of cancer had serum iron levels tested at the time of recruitment (1997–2008). Initially measured iron levels were associated with subsequent cancer risk by linking individuals with the National Cancer Registry and National Death File. HRs were calculated by the Cox model. One third of males (35%) and one fifth of females (18%) had high serum iron (≥120 μg/dL), which was associated with a 25% increase in risk for incidence of all cancers [HR, 1.25; 95% confidence interval (CI), 1.16–1.35] and with a 39% increase in risk for mortality from all cancers (HR, 1.39; 95% CI, 1.23–1.57). The relationship between serum iron and cancer risk was a J-shaped one, with higher cancer risk at both ends, either at lower than 60 μg/dL or higher than 120 μg/dL. At the higher end, cancer risk increased by 4% for every 10 μg/dL increment above 80 μg/dL, showing a dose–response relationship, with 60 to 79 μg/dL as a reference level. In a sensitivity analysis, the increases in risk were still observed after the first 5 years of cancer cases were excluded. Liver cancer risk was increased in HBV (−) non-hepatitis B carrier (3-fold) and HBV (+) hepatitis B carrier (24-fold). Lifestyle risks such as smoking, drinking, or inactivity interacted synergistically with high serum iron and significantly increased the cancer risks. The liver (HR, 2.49; 95% CI, 1.97–3.16) and the breast (HR, 1.31; 95% CI, 1.01–1.70) were the two major cancer sites where significant cancer risks were observed for serum iron either ≥120 μg/dL or ≥140 μg/dL, respectively. This study reveals that high serum iron is both a common disorder and a marker of increased risk for several cancers. Cancer Res; 74(22); 6589–97. ©2014 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 4
    Online Resource
    Online Resource
    Microbiology Society ; 2011
    In:  Journal of General Virology Vol. 92, No. 11 ( 2011-11-01), p. 2637-2645
    In: Journal of General Virology, Microbiology Society, Vol. 92, No. 11 ( 2011-11-01), p. 2637-2645
    Abstract: BK virus (BKV) infection may cause polyomavirus-associated nephropathy in patients with renal transplantation. Recently, the phosphorylated amino acids on the structural proteins VP1, VP2 and VP3 of BKV have been identified by liquid chromatography–tandem mass spectrometry in our laboratory. In this study, we further analysed the biological effects of these phosphorylation events. Phosphorylation of the BKV structural proteins was demonstrated by [ 32 P]orthophosphate labelling in vivo . Site-directed mutagenesis was performed to replace all of the phosphorylated amino acids. The mutated BKV genomes were transfected into Vero cells for propagation analysis. The results showed that expression of the early protein LT and of the late protein VP1 by the mutants VP1-S80A, VP1-S80-133A, VP1-S80-327A, VP1-S80-133-327A and VP2-S254A was abolished. However, propagation of other mutants was similar to that of wild-type BKV. The results suggest that phosphorylation of Ser-80 of VP1 and Ser-254 of VP2 is crucial for BKV propagation.
    Type of Medium: Online Resource
    ISSN: 0022-1317 , 1465-2099
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    Language: English
    Publisher: Microbiology Society
    Publication Date: 2011
    detail.hit.zdb_id: 2007065-2
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. LB-324-LB-324
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. LB-324-LB-324
    Abstract: Background: Attention has been focused on the increased risk of high cholesterol, but the effect of low cholesterol remains unclear and receives little attention. Method: The study cohort, 537,430 adults in Taiwan who went through a medical screening program between 1996 and 2008, was followed up for an average of 8.5 years for mortality and cancer incidence, with 18,745 deaths and 17,714 cancer cases identified. Low and very low cholesterol or LDL were defined as & lt; 180 and & lt;160, or & lt;110 and & lt;90 mg/dL, respectively. Cox proportionate model was used for hazard ratio (HR) calculation, by controlling for all relevant risk factors (Age, gender, BMI, smoking, drinking, blood pressure, blood sugar, physical activity and anemia) Results: One out of four (24.6%) had low cholesterol and 7.5% had very low cholesterol, in contrast to 10.4% with high cholesterol. Increases in all cancer mortality were found for those with low cholesterol (HR:1.41, with 95% 1.3-1.5) and very low cholesterol (HR: 1.58 with 95% 1.4-1.7), with 180-239 mg/dL as reference. Similar results were seen for cancer incidence. The increase came prominently from liver cancer (HR:2.86), and the increases remained after all deaths or all cancer incidences within the first 3 years were excluded (HR: 1.31), or after HBV carriers were excluded (HR: 1.33). All cancer mortality increased by 1% for every unit decrease of cholesterol across all levels. With 60% increase in all-cause mortality, the life span of very low cholesterol was shortened by 5-6 years. Conclusion: Found in 1/4 of adult Asians, subjects with low cholesterol ( & lt;180 mg/dL), a level commonly reached by those taking statins or on vegetarian diet, had approximately 50% increase in cancer risks. The inverse relationship existed across all levels of cholesterol, with 10% increase for every 10-unit decrease. Those with very low cholesterol had their life span shortened by 5-6 years. While reverse causation with pre-clinical cancer cases could be responsible, the fact that the cancer risks remained after excluding first three years of cancer implied low cholesterol is an independent risk factor or risk marker for all cancer. In this Asian community, low cholesterol should receive as much attention as high cholesterol. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr LB-324. doi:1538-7445.AM2012-LB-324
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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