Worldwide variations in colorectal cancer. CA Cancer J Clin

Department of Surveillance and Health Policy Research, American Cancer Society, 250 Williams Street NW, Atlanta, GA 30303, USA.
CA A Cancer Journal for Clinicians (Impact Factor: 115.84). 11/2009; 59(6):366-78. DOI: 10.3322/caac.20038
Source: PubMed


Previous studies have documented significant international variations in colorectal cancer rates. However, these studies were limited because they were based on old data or examined only incidence or mortality data. In this article, the colorectal cancer burden and patterns worldwide are described using the most recently updated cancer incidence and mortality data available from the International Agency for Research on Cancer (IARC). The authors provide 5-year (1998-2002), age-standardized colorectal cancer incidence rates for select cancer registries in IARC's Cancer Incidence in Five Continents, and trends in age-standardized death rates by single calendar year for select countries in the World Health Organization mortality database. In addition, available information regarding worldwide colorectal cancer screening initiatives are presented. The highest colorectal cancer incidence rates in 1998-2002 were observed in registries from North America, Oceania, and Europe, including Eastern European countries. These high rates are most likely the result of increases in risk factors associated with "Westernization," such as obesity and physical inactivity. In contrast, the lowest colorectal cancer incidence rates were observed from registries in Asia, Africa, and South America. Colorectal cancer mortality rates have declined in many longstanding as well as newly economically developed countries; however, they continue to increase in some low-resource countries of South America and Eastern Europe. Various screening options for colorectal cancer are available and further international consideration of targeted screening programs and/or recommendations could help alleviate the burden of colorectal cancer worldwide.

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    • "Colorectal cancer is one of the most common malignancies in the world, as the third most common cancer in men and the second in women [1]. Although colorectal cancer incidence rates are stabilizing or even declining in historically high-risk areas (United States, New Zealand, and Canada), they are rapidly increasing in several historically low-risk countries (China, Japan, Korea, and Eastern European countries) [2] [3]. Colorectal cancer mainly results from a series of genetic changes leading to the progressive and irreversible loss of the normal control of cell growth and differentiation [4]. "
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    ABSTRACT: Antibody-based imaging agents are attractive as adjuvant diagnostic tools for solid tumors. GPA33 is highly expressed in most human colorectal cancers and has been verified as a diagnostic and therapeutic target. Here, we built an A33scFv-Fc antibody against GPA33 by fusing A33scFv to the Fc fragment of human IgG1 antibodies. The A33scFv-Fc specifically binds GPA33-positive colorectal cancer cells and tumor tissues. After the intravenous injection of mice bearing subcutaneous GPA33-positive LS174T tumor grafts with near-infrared fluorescence probe CF750-labeled A33scFv-Fc (CF750-A33scFv-Fc), high contrast images of the tumor grafts could be kinetically documented within 24 h using an optical imaging system. However, GPA33-negative SMMC7721 tumor grafts could not be visualized by injecting the same amount of CF750-A33scFv-Fc. Moreover, in subcutaneous LS174T tumor-bearing mice, tissue scanning revealed that the CF750-A33scFv-Fc accumulated in the tumor grafts, other than the kidney and liver. In mice with orthotopic tumor transplantations, excrescent LS174T tumor tissues in the colon were successfully removed under guidance by CF750-A33scFv-Fc-based optical imaging. These results indicate that CF750-A33scFv-Fc can target GPA33, suggesting the potential of CF750-A33scFv-Fc as an imaging agent for the diagnosis of colorectal cancer.
    06/2015; 2015:1-11. DOI:10.1155/2015/505183
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    • "Garland et al. demonstrated an inverse correlation between dietary calcium (Ca 2+ ) intake and the risk of colorectal cancer (CRC), identifying nutritional Ca 2+ as a promising chemopreventive agent [1]. Since then several advances have been made with focus on studies trying to establish risk factors to facilitate suitable intervention in CRC [1] [2] [3]. "
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    ABSTRACT: An inverse correlation between dietary calcium intake and the risk of colorectal cancer (CRC) is well known, but poorly understood. Expression of the calcium-sensing receptor (CaSR), a calcium-binding G protein-coupled receptor is downregulated in CRC leading us to hypothesize that the CaSR has tumor suppressive roles in the colon. The aim of this study was to understand whether restoration of CaSR expression could reduce the malignant phenotype in CRC. In human colorectal tumors, expression of the CaSR negatively correlated with proliferation markers whereas loss of CaSR correlated with poor tumor differentiation and reduced apoptotic potential. In vivo, dearth of CaSR significantly increased expression of proliferation markers and decreased levels of differentiation and apoptotic markers in the colons of CaSR/PTH double knock-out mice confirming the tumor suppressive functions of CaSR. To prove that normally functioning CaSR is indeed important to maintain the balance between proliferation-differentiation-apoptosis, we extended the study in vitro. CRC cells stably overexpressing wild-type CaSR showed significant reduction in proliferation, as well as increased differentiation and apoptotic potential. The positive allosteric modulator of CaSR, NPS R-568 further enhanced these effects, whereas treatment with the negative allosteric modulator, NPS 2143 inhibited these functions. Interestingly, the dominant-negative mutant (R185Q) was able to abrogate the effects of calcium. Our results demonstrate a critical tumor suppressive role of CaSR in the colon. Restoration of CaSR expression and function is linked to regulation of the balance between proliferation, differentiation, and apoptosis and provides a rationale for novel strategies in CRC therapy. Copyright © 2015 The Authors. Published by Elsevier B.V. All rights reserved.
    Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 02/2015; 1(9). DOI:10.1016/j.bbamcr.2015.02.011 · 5.02 Impact Factor
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    • "CRC is the third most common cancer and the number one cause of nonsmoking cancer-related deaths in the world (Ferlay et al., 2010). Globally, there is a wide variability in the incidence of CRC, with the highest incidence in Australia, New Zealand, Europe and North America, and the lowest in Africa and Asia (Center et al., 2009; Jemal et al., 2011). Although developing countries historically have a low rate of CRC, a recent study by Chalya et al. (2013) revealed that CRC is reported to be increasing in resource-limited countries, probably due to the acquisition of a western lifestyle. "
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    ABSTRACT: The aim of this study was to investigate the antiproliferative and protective effects of the brown seaweeds, Turbinaria ornata and Padina pavonia, against azoxymethane (AOM)-induced colon carcinogenesis in mice. Both algal extracts showed anti-proliferative effects on the human carcinoma cell line HCT-116 in vitro, with T. ornata demonstrating a more potent effect. Male albino Swiss mice received intraperitoneal injections of AOM (10 mg/kg) once a week for two consecutive weeks and 100 mg/kg of either T. ornata or P. pavonia extracts. AOM-induced mice exhibited alterations in the histological structure of the colon, elevated lipid peroxidation and nitric oxide, declined glutathione content and reduced activity of superoxide dismutase and glutathione peroxidase. In addition, AOM induced downregulation of peroxisome proliferator activated receptor gamma (PPARγ) and p53 mRNA expression, with concomitant upregulation of nuclear factor-kappa B (NF-κB) in colon tissue. Administration of either algal extract markedly alleviated the recorded alterations. In conclusion, the current study suggests that T. ornata and P. pavonia, through their antioxidant and anti-inflammatory effects, are able to attenuate colon inflammation by downregulating NF-κB expression. Furthermore, the protective effects of both algae against AOM-initiated carcinogenesis were attributed, at least in part, to their ability to upregulate colonic PPARγ and p53 expression. Copyright © 2015 John Wiley & Sons, Ltd. Copyright © 2015 John Wiley & Sons, Ltd.
    Phytotherapy Research 02/2015; DOI:10.1002/ptr.5310 · 2.66 Impact Factor
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