The growing incidence of cancer: role of lifestyle and screening detection (Review).
ABSTRACT The increasing incidence of a variety of cancers after the Second World War confronts scientists with the question of their origin. In Western countries, expansion and ageing of the population, as well as progress in cancer detection using new diagnostic and screening tests cannot fully account for the observed growing incidence of cancer. Our hypothesis is that environmental factors play a more important role in cancer genesis than it is usually agreed: i) over the last 2-3 decades, alcohol consumption and tobacco smoking in men have significantly decreased; ii) obesity is increasing in many countries, but the growing incidence of cancer also concerns cancers not related to obesity nor to other lifestyle-related factors; iii) there is evidence that the environment has changed over the same time scale as the recent rise in cancer incidence, and that this change included the accumulation of many new carcinogenic factors in the environment; iv) genetic susceptibility to cancer due to genetic polymorphism cannot have changed over one generation and actually favours the role of exogenous factors through gene-environment interactions; v) age is not the unique factor to be considered since the rising incidence of cancers is seen across all age categories, including children; vi) the fetus is specifically vulnerable to exogenous factors. A fetal exposure during a critical window period may explain why current epidemiological studies may be negative in adults. We therefore propose that the involuntary exposure to many carcinogens in the environment contributes to the rising trend in cancer incidence.
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ABSTRACT: This article challenges the idea that cancer cannot be prevented among older adults by examining different aspects of the relationship between age and cancer. Although the sequential patterns of aging cannot be changed, several age-related factors that contribute to disease risk can be. For most adults, age is coincidentally associated with preventable chronic conditions, avoidable exposures, and modifiable risk behaviors that are causally associated with cancer. Midlife is a period of life when the prevalence of multiple cancer risk factors is high and incidence rates begin to increase for many types of cancer. However, current evidence suggests that for most adults, cancer does not have to be an inevitable consequence of growing older. Interventions that support healthy environments, help people manage chronic conditions, and promote healthy behaviors may help people make a healthier transition from midlife to older age and reduce the likelihood of developing cancer. Because the number of adults reaching older ages is increasing rapidly, the number of new cancer cases will also increase if current incidence rates remain unchanged. Thus, the need to translate the available research into practice to promote cancer prevention, especially for adults at midlife, has never been greater.American journal of preventive medicine 03/2014; 46(3 Suppl 1):S7-S15. DOI:10.1016/j.amepre.2013.10.029 · 4.28 Impact Factor
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ABSTRACT: Although the connection between cancer and cigarette smoke is well established, nicotine is not characterized as a carcinogen. Here, we used exome sequencing to identify nicotine and oxidative stress-induced somatic mutations in normal human epithelial cells and its correlation with cancer. We identified over 6,400 SNVs, indels and microsatellites in each of the stress exposed cells relative to the control, of which, 2,159 were consistently observed at all nicotine doses. These included 429 nsSNVs including 158 novel and 79 cancer-associated. Over 80% of consistently nicotine induced variants overlap with variations detected in oxidative stressed cells, indicating that nicotine induced genomic alterations could be mediated through oxidative stress. Nicotine induced mutations were distributed across 1,585 genes, of which 49% were associated with cancer. MUC family genes were among the top mutated genes. Analysis of 591 lung carcinoma tumor exomes from The Cancer Genome Atlas (TCGA) revealed that 20% of non-small-cell lung cancer tumors in smokers have mutations in at least one of the MUC4, MUC6 or MUC12 genes in contrast to only 6% in non-smokers. These results indicate that nicotine induces genomic variations, promotes instability potentially mediated by oxidative stress, implicating nicotine in carcinogenesis, and establishes MUC genes as potential targets.Oncotarget 05/2014; 5(13). · 6.63 Impact Factor
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ABSTRACT: KRAS mutation is frequently detected in a series of cancers, including papillary thyroid cancer (PTC). Recently, a genetic variant of rs712 in the 3' untranslated region of the KRAS gene has been reported to be functional in the regulation of KRAS by disrupting complementary site of let-7 and miR-181. We aimed to investigate whether the polymorphism is a risk factor for PTC. We conducted an association study, including 252 PTC patients and 290 healthy controls. The KRAS rs712 polymorphism was genotyped by polymerase chain reaction-restriction fragment length polymorphism. Although no significant difference of the KRAS rs712 distribution was observed between cases and controls in overall analysis, stratification analysis showed that patients carrying the KRAS rs712TT genotype were less likely to develop stages T3 and T4 under a recessive genetic model (OR 0.26, 95 % CI 0.08-0.82). These results supported the role of the KRAS rs712 polymorphism as a potential genetic biomarker for the extension of PTC. Further population-based association studies are of great value to confirm the results in diverse ethnicities.Medical Oncology 10/2014; 31(10):221. DOI:10.1007/s12032-014-0221-3 · 2.06 Impact Factor