Youlden DR, Cramb SM, Dunn NA, Muller JM, Pyke CM, Baade PDThe descriptive epidemiology of female breast cancer: an international comparison of screening, incidence, survival and mortality. Cancer Epidemiol 36: 237-248

Viertel Centre for Research in Cancer Control, Cancer Council Queensland, Spring Hill, Qld 4004, Australia.
Cancer epidemiology 03/2012; 36(3):237-48. DOI: 10.1016/j.canep.2012.02.007
Source: PubMed


This paper presents the latest international descriptive epidemiological data for invasive breast cancer amongst women, including incidence, survival and mortality, as well as information on mammographic screening programmes.
Almost 1.4 million women were diagnosed with breast cancer worldwide in 2008 and approximately 459,000 deaths were recorded. Incidence rates were much higher in more developed countries compared to less developed countries (71.7/100,000 and 29.3/100,000 respectively, adjusted to the World 2000 Standard Population) whereas the corresponding mortality rates were 17.1/100,000 and 11.8/100,000. Five-year relative survival estimates range from 12% in parts of Africa to almost 90% in the United States, Australia and Canada, with the differential linked to a combination of early detection, access to treatment services and cultural barriers. Observed improvements in breast cancer survival in more developed parts of the world over recent decades have been attributed to the introduction of population-based screening using mammography and the systemic use of adjuvant therapies.
The future worldwide breast cancer burden will be strongly influenced by large predicted rises in incidence throughout parts of Asia due to an increasingly "westernised" lifestyle. Efforts are underway to reduce the global disparities in survival for women with breast cancer using cost-effective interventions.

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    • "BC is the second most common cancer and the fifth leading cause of cancer deaths worldwide. In 2008, approximately 1.4 million women were diagnosed with BC, and approximately 459,000 deaths were reported in worldwide [1]. In 2008, it was the most prevalent cancer and the fourth leading cause of cancer-related deaths in Taiwan [2]. "
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    ABSTRACT: APOE ε2 or ε4 alleles being used as indicators of breast cancer risk are controversial in Taiwanese females. We provide a concept for relative comparisons of post-translational modifications (PTMs) of plasma apolipoprotein E (ApoE) between normal controls and breast cancer patients to investigate the association of ApoE with breast cancer risk. APOE polymorphisms (ApoE isoforms) were not assessed in this study. The relative modification ratio (%) of 15 targeted and 21 modified peptides were evaluated by 1D SDS-PAGE, in-gel digestion, and label-free nano-LC/MS to compare normal controls with breast cancer patients. Plasma levels of the ApoE protein did not significantly differ between normal controls and breast cancer patients. Eleven sites with novel PTMs were identified from 7 pairs of differentially expressed targeted and modified peptides according to the relative modification ratio including methylation at the E3 (↑1.45-fold), E7 (↑1.45-fold), E11 (↑1.19-fold), E77 (↑2.02-fold), E87 (↑2.02-fold), and Q98 (↑1.62-fold) residues; dimethylation at the Q187 (↑1.44-fold) residue; dihydroxylation at the R92 (↑1.25-fold), K95 (↑1.25-fold), and R103 (↑1.25-fold) residues; and glycosylation at the S129 (↑1.14-fold) residue. The clustered methylation and dihydroxylation of plasma ApoE proteins may play a role in breast cancer.
    Journal of proteomics 06/2015; 126. DOI:10.1016/j.jprot.2015.05.038 · 3.89 Impact Factor
    • "Breast cancer is the most common cancer in women and a leading cause of cancer mortality worldwide (Jemal et al., 2011; Youlden et al., 2012). The majority of breast cancers are estrogen receptor (ER)– positive and depend on ER signaling for their proliferation (Miller et al., 2008). "
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    ABSTRACT: We previously reported upregulation of UGT2B15 by 17β-estradiol in breast cancer MCF7 cells via the binding of the estrogen receptor alpha (ERα) to an estrogen-response unit (ERU) in the proximal UGT2B15 promoter. In the present study, we show that this ERα-mediated upregulation was significantly reduced by two ER antagonists (fulvestrant and raloxifene) but not affected by a third ER antagonist, 4-hydroxy-tamoxifen (4-OHTAM), a major active tamoxifen (TAM) metabolite. Furthermore, we found that, similar to 17β-estradiol, 4-OHTAM and endoxifen (another major active TAM metabolite) elevated UGT2B15 mRNA levels, and that this stimulation was significantly abrogated by fulvestrant. Further experiments using 4-OHTAM revealed a critical role for ERα in this regulation. Specifically, knockdown of ERα expression by anti-ERα siRNA reduced the 4-OHTAM-mediated induction of UGT2B15 expression; 4-OHTAM activated the wild-type but not the ERU-mutated UGT2B15 promoter; chromatin immunoprecipitation (ChIP) assays showed increased ERα occupancy at the UGT2B15 ERU in MCF7 cells upon exposure to 4-OHTAM. Together, these data indicate that both 17β-estradiol and the antiestrogen 4-OHTAM upregulate UGT2B15 in MCF7 cells via the same ERα-signalling pathway. This is consistent with previous observations that both 17β-estradiol and TAM upregulate a common set of genes in MCF7 cells via the ER signalling pathway. As 4-OHTAM is a UGT2B15 substrate, the upregulation of UGT2B15 by 4-OHTAM in target breast cancer cells is likely to enhance local metabolism and inactivation of 4-OHTAM within the tumour. This represents a potential mechanism that may reduce TAM therapeutic efficacy or even contribute to the development of acquired TAM resistance. The American Society for Pharmacology and Experimental Therapeutics.
    Drug metabolism and disposition: the biological fate of chemicals 03/2015; 43(6). DOI:10.1124/dmd.114.062935 · 3.25 Impact Factor
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    • "Chemotherapy, radiotherapy and endocrine therapy also play important roles in breast cancer. Although with comprehensive therapy, there are about 0.5 million women patients died of breast cancer each year due to recurrence, metastasis and resistance to therapy [2]. Therefore, more effective therapeutic strategies are required to improve treatment outcomes for breast cancer patients. "
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    ABSTRACT: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can selectively induce apoptosis of cancer cells and is verified effective to various cancers. However, a variety of breast cancer cell lines are resistant to TRAIL and the mechanisms of resistance are largely unknown. In our present experiment, we successfully utilized breast cancer cell line MDA-MB-231 to establish TRAIL-resistant cell line. We found resistance to TRAIL could induce epithelial-mesenchymal transition (EMT) and enhance invasiveness. We further demonstrated PTEN was down-regulated in TRAIL-resistant cells. Silencing miR-221, PTEN expression was up-regulated, the process of EMT could be reversed, and the ability of migration and invasion were correspondingly weakened. We also demonstrated knockdown of miR-221 could reverse resistance to TRAIL partially by targeting PTEN. Our findings suggest that resistance to TRAIL could induce EMT and enhance invasiveness by suppressing PTEN via miR-221. Re-expression of miR-221 or targeting PTEN might serve as potential therapeutic approaches for the treatment of Trail-resistant breast cancer.
    PLoS ONE 06/2014; 9(6):e99067. DOI:10.1371/journal.pone.0099067 · 3.23 Impact Factor
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