Opportunities for cancer epidemiology in developing countries
Division of Cancer Epidemiology & Genetics, National Cancer Institute, NIH, DHHS, 6120 Executive Boulevard, Rockville, Maryland 20852, USA.Nature reviews. Cancer (Impact Factor: 37.4). 12/2004; 4(11):909-17. DOI: 10.1038/nrc1475
Most cancer epidemiology studies involve people living in North America and Europe, which represent only a fraction of the global population. The wide variety of dietary, lifestyle and environmental exposures, as well as the genetic variation among people in developing countries can provide valuable new information on factors that contribute to cancer or that protect against it. What are the challenges and advantages to performing large epidemiological studies in developing nations?
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- "Cancer is presently a worldwide health problem and the leading cause of death in the United States and other developed countries (Rastogi et al., 2004). Cancer is a formidable disease caused by disordered cell growth and invasion of tissues and organs. "
ABSTRACT: Background and purpose: 4-Phenylquinolin-2(1H)-one (4-PQ) derivatives can induce cancer cell apoptosis. Additional new 4-PQ analogs were investigated as more effective, less toxic antitumour agents. Experimental approach: Forty-five 6,7,8-substituted 4-substituted benzyloxyquinolin-2(1H)-one derivatives were synthesized. Antiproliferative activities were evaluated using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliun bromide assay and structure-activity relationship correlations were established. Compounds 9b, 9c, 9e and 11e were also evaluated against the National Cancer Institute-60 human cancer cell line panel. Hoechst 33258 and Annexin V-FITC/PI staining assays were used to detect apoptosis, while inhibition of microtubule polymerization was assayed by fluorescence microscopy. Effects on the cell cycle were assessed by flow cytometry and on apoptosis-related proteins (active caspase-3, -8 and -9, procaspase-3, -8, -9, PARP, Bid, Bcl-xL and Bcl-2) by Western blotting. Key results: Nine 6,7,8-substituted 4-substituted benzyloxyquinolin-2(1H)-one derivatives (7e, 8e, 9b, 9c, 9e, 10c, 10e, 11c and 11e) displayed high potency against HL-60, Hep3B, H460, and COLO 205 cancer cells (IC₅₀ < 1 μM) without affecting Detroit 551 normal human cells (IC₅₀ > 50 μM). Particularly, compound 11e exhibited nanomolar potency against COLO 205 cancer cells. Mechanistic studies indicated that compound 11e disrupted microtubule assembly and induced G2/M arrest, polyploidy and apoptosis via the intrinsic and extrinsic signalling pathways. Activation of JNK could play a role in TRAIL-induced COLO 205 apoptosis. Conclusion and implications: New quinolone derivatives were identified as potential pro-apoptotic agents. Compound 11e could be a promising lead compound for future antitumour agent development.
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- "The HPV variants are known to affect virus assembly , immunologic responses, pathogenicity, p53 degradation , immortalization activity, and regulation of transcription [Kirnbauer et al., 1993; Kast et al., 1994; Ellis et al., 1995; Hildesheim et al., 2001; Veress et al., 2001; Rastogi et al., 2004]. Of the two oncogenes E6 and E7, E6 has shown more variations than E7, which is conserved relatively [Yamada et al., 1997; Zehbe et al., 1998a,b; van Duin et al., 2000; Tornesello et al., 2004]. "
ABSTRACT: High-risk human papillomavirus (HPV) types, specifically HPV 16 E6 variants are involved in viral persistence and the development of cervical lesions. India contributes to 1/3rd of the global cervical cancer deaths; however, information on E6 variants in the Indian population is limited. Information on these variants is essential for successful implementation of cervical cancer immunization programs. The E6 variants and their possible biological implications to the outcome of infection were studied in women attending the Tata Memorial Hospital, Mumbai, India. Cervical cancer patients with HPV 16 as a single infection (n = 33), co-infection with another HPV type (n = 20) or with multiple types (n = 10) were examined for HPV16 E6 variants using PCR and sequence analysis. The variants were identified using the prototype sequence (HPV 16R) belonging to the European lineage. The results revealed that the European T350G was the most common variant (50%) followed by the European prototype (40.3%) and the North-American (N = 3; 4.8%). The European prototype was significantly more frequent in patients infected with HPV16 alone (P < 0.05, C.I. 1.2–13.6), while the European T350G variants were seen in women with co-infections. The North-American lineage was found in women infected with HPV16 and 33. Three novel variants were identified of which two were non-synonymous. Phylogenetic analysis revealed that the variant F69L + L83V is not related to any of these lineages, while the variant M137L + L83V is closely related to the North American variant. This study found a difference in the prevalence of E6 variants compared to earlier Indian studies and their association with type of infection. J. Med. Virol. © 2014 Wiley Periodicals, Inc.
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- "Colorectal cancer is the third most common malignancy in Western countries1 and in South Korea.2 Despite remarkable advances in diagnostic and therapeutic modalities, 20% of patients are still diagnosed with colorectal cancer at a far advanced stage, with distant metastasis, and these patients have a 5-year survival rate of only 12%.3 "
ABSTRACT: Purpose The dipeptidyl peptidase IV (DPPIV) gene family exhibits multiple functions and is involved in the pathogenesis of various diseases. It has attracted pharmaceutical interest in the areas of metabolic disorders as well as cancer. However, clinicopathologic significance of DPPIV family in colorectal cancer is not fully understood. Materials and Methods The clinical relevance of DPPIV and DPP10 expression was determined by immunohistochemical staining, and by assessing its clinicopathologic correlation in 383 colorectal cancer patients with known clinical outcomes. Results DPPIV was not expressed in normal colon mucosa, but it showed luminal expression in 52 of the 383 colorectal cancers (13.5%). DPPIV expression in tumors was associated with right-sided location of the colon (p=0.010) and more advanced tumor stage (p=0.045). DPP10 was expressed in normal colonic mucosa, but its expression varied in primary colorectal cancer tissues. Loss of DPP10 expression was found in 11 colorectal cancers (CRCs) (2.9%), and multivariate analysis showed that loss of DPP10 expression was an independent factor for poor patient prognosis (p=0.008). Conclusion DPP10 may play a role in disease progression of colorectal cancer and loss of DPP10 expression in primary CRC is significantly associated with poor survival outcomes.
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