Global cancer statistics. CA. Cancer J Clin

Surveillance Research, American Cancer Society, Atlanta, GA, USA.
CA A Cancer Journal for Clinicians (Impact Factor: 162.5). 02/2011; 61(2):69-90. DOI: 10.3322/caac.20107
Source: PubMed

ABSTRACT The global burden of cancer continues to increase largely because of the aging and growth of the world population alongside an increasing adoption of cancer-causing behaviors, particularly smoking, in economically developing countries. Based on the GLOBOCAN 2008 estimates, about 12.7 million cancer cases and 7.6 million cancer deaths are estimated to have occurred in 2008; of these, 56% of the cases and 64% of the deaths occurred in the economically developing world. Breast cancer is the most frequently diagnosed cancer and the leading cause of cancer death among females, accounting for 23% of the total cancer cases and 14% of the cancer deaths. Lung cancer is the leading cancer site in males, comprising 17% of the total new cancer cases and 23% of the total cancer deaths. Breast cancer is now also the leading cause of cancer death among females in economically developing countries, a shift from the previous decade during which the most common cause of cancer death was cervical cancer. Further, the mortality burden for lung cancer among females in developing countries is as high as the burden for cervical cancer, with each accounting for 11% of the total female cancer deaths. Although overall cancer incidence rates in the developing world are half those seen in the developed world in both sexes, the overall cancer mortality rates are generally similar. Cancer survival tends to be poorer in developing countries, most likely because of a combination of a late stage at diagnosis and limited access to timely and standard treatment. A substantial proportion of the worldwide burden of cancer could be prevented through the application of existing cancer control knowledge and by implementing programs for tobacco control, vaccination (for liver and cervical cancers), and early detection and treatment, as well as public health campaigns promoting physical activity and a healthier dietary intake. Clinicians, public health professionals, and policy makers can play an active role in accelerating the application of such interventions globally.

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    • "Hepatocellular carcinoma (HCC) is the most common type of liver cancer and the third cause of cancer-related mortality worldwide (Jemal et al. 2011). HCC is generally diagnosed at a late stage, and the majority of HCC patients die within 1 year after diagnosis. "
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    ABSTRACT: Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death worldwide. The multityrosine kinase inhibitor sorafenib is used in the therapy of advanced disease. However, the effects of sorafenib are limited, and combination treatments aiming at improved survival are encouraged. The sphingosine analog FTY720 (Fingolimod), which is approved for treatment of multiple sclerosis, has shown tumor suppressive effects in cell lines and animal models of HCC. In the present study, we combined sorafenib with FTY720 in order to sensitize the HCC cell lines Huh7 and HepG2 to sorafenib treatment. Using the XTT assay we show that noncytotoxic doses of FTY720 synergistically enhanced the decrease in viability caused by treatment of both cell lines with increasing doses of sorafenib. Further studies in Huh7 revealed that combined treatment with FTY720 and sorafenib resulted in G1 arrest and enhanced cell death measured using flow cytometry analysis of cells labeled with propidium iodide (PI)/Annexin-V and PI and 4′,6-diamidino-2-phenylindole-staining of nuclei. In addition, signs of both caspase-dependent and – independent apoptosis were observed, as cotreatment with FTY720 and sorafenib caused cytochrome c release and poly-ADP ribose polymerase-cleavage as well as translocation of Apoptosis-inducing factor into the cytosol. We also detected features of autophagy blockage, as the protein levels of LC3-II and p62 were affected by combined treatment with FTY720 and sorafenib. Together, our results suggest that FTY720 sensitizes HCC cells to cytotoxic effects induced by treatment with sorafenib alone. These findings warrant further investigations of combined treatment with sorafenib and FTY720 in vivo in order to develop more effective treatment of HCC.
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    • "GC is one of the most common human malignant cancers worldwide, about one million new GC cases and 723,000 deaths are estimated to have occurred in 2012, accounting for 8% of the total cases and 10% of total deaths (http:// Over 70% of new cases and deaths occur in developing countries (Jemal et al., 2011). Many miRNAs were reported to be associated with GC development in the past decade, including miR-146a (Yao et al., 2013), miR-204-5p (Zhang et al., 2015), miR-486 (Oh et al., 2011), miR-192 (Jin et al., 2011), miR-215 (Jin et al., 2011), "
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    ABSTRACT: MicroRNAs (miRNAs) are a type of small non-coding RNAs that are often play important roles in carcinogenesis, but the carcinogenic mechanism of miRNAs is still unclear. This study will investigate the function and the mechanism of miR-638 in carcinoma (GC). The expression of miR-638 in GC and the DNA copy number of miR-638 were detected by real-time PCR. The effect of miR-638 on cell proliferation was measured by counting kit-8 assay. Different assays, including bioinformatics algorithms (TargetScan and miRanda), luciferase report assay and Western blotting, were used to identify the target gene of miR-638 in GC. The expression of miR-638 target gene in clinical CRC tissues was also validated by immunohistochemical assay. From this research, we found that miR-638 was downregulated in GC tissues compared with corresponding noncancerous tissues (NCTs), and the DNA copy number of miR-638 was lower in GC than NCTs, which may induce the corresponding downregulation of miR-638 in GC. Ectopic expression of miR-638 inhibited GC cell growth in vitro. Subsequently, we identified that PLD1 is the target gene of miR-638 in GC, and silencing PLD1 expression phenocopied the inhibitory effect of miR-638 on GC cell proliferation. Furthermore, we observed that PLD1 was overexpressed in GC tissues, and high expression of PLD1 in GC predicted poor overall survival. In summary, we revealed that miR-638 functions as a tumor suppressor in GC through inhibiting PLD1.
    Protein & Cell 08/2015; DOI:10.1007/s13238-015-0187-8 · 2.85 Impact Factor
    • "Head and neck cancer (HNC) is a group of cancers including cancer of the oral cavity, pharynx, larynx and oropharynx . HNC is the sixth most common cancer in the world, (Jemal et al. 2011). Annually, nearly 140 000 people are diagnosed with HNC in Europe (EUCAN 2012); and over 1300 people are diagnosed with HNC in Scotland (NHS Scotland 2012). "
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    ABSTRACT: The aim of this study was to identify the distress, unmet needs and concerns of head and neck cancer (HNC) survivors in the first 5 years after treatment. Two hundred and eighty HNC survivors from three Scottish health boards responded to a cross-sectional postal survey in 2011. Questionnaires included the Distress Thermometer, Patient Concerns Inventory (PCI) and an adapted version of the PCI to measure unmet needs. One-third of the survivors had moderate or severe levels of distress, and 74% had at least one unmet need. The most common concerns and unmet needs included oral and eating problems, fear of recurrence and fatigue. Multivariate analysis revealed that being younger, out of work (not retired), ever having had a feeding tube fitted, having a greater number of comorbidities and living alone were associated with higher levels of distress, concerns and unmet needs. The diversity of concerns and unmet needs identified in this study highlights the importance of holistic needs assessment as part of follow-up care for HNC survivors with tailoring of support for particular concerns. Specific information resources and self-management strategies are required to help HNC survivors with the practical and functional consequences of HNC treatment. © 2015 John Wiley & Sons Ltd.
    European Journal of Cancer Care 07/2015; DOI:10.111/ecc.12370 · 1.76 Impact Factor
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