Lifestyle-related factors and environmental agents causing cancer: An overview

Cancer Research Center, Association for Research and Treatments Against Cancer (ARTAC), 57-59 Rue de la Convention, 75015 Paris, France.
Biomedecine [?] Pharmacotherapy (Impact Factor: 2.02). 01/2008; 61(10):640-58. DOI: 10.1016/j.biopha.2007.10.006
Source: PubMed


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. (1) Over the last 2-3 decades, alcohol consumption and tobacco smoking in men have significantly decreased in Western Europe and North America. (2) Obesity is increasing in many countries, but the growing incidence of cancer also concerns cancers not related to obesity nor to other known lifestyle-related factors. (3) There is evidence that the environment has changed over the time period preceding the recent rise in cancer incidence, and that this change, still continuing, included the accumulation of many new carcinogenic factors in the environment. (4) 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. (5) Age is not the unique factor to be considered since the rising incidence of cancers is seen across all age categories, including children, and adolescents. (6) The fetus is specifically vulnerable to exogenous factors. A fetal exposure during a critical time window may explain why current epidemiological studies may still be negative in adults. We therefore propose that the involuntary exposure to many carcinogens in the environment, including microorganisms (viruses, bacteria and parasites), radiations (radioactivity, UV and pulsed electromagnetic fields) and many xenochemicals, may account for the recent growing incidence of cancer and therefore that the risk attributable to environmental carcinogen may be far higher than it is usually agreed. Of major concern are: outdoor air pollution by carbon particles associated with polycyclic aromatic hydrocarbons; indoor air pollution by environmental tobacco smoke, formaldehyde and volatile organic compounds such as benzene and 1,3 butadiene, which may particularly affect children and food contamination by food additives and by carcinogenic contaminants such as nitrates, pesticides, dioxins and other organochlorines. In addition, carcinogenic metals and metalloids, pharmaceutical medicines and some ingredients and contaminants in cosmetics may be involved. Although the risk fraction attributable to environmental factors is still unknown, this long list of carcinogenic and especially mutagenic factors supports our working hypothesis according to which numerous cancers may in fact be caused by the recent modification of our environment.

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Available from: Philippe Irigaray, Jul 25, 2014
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    • "Ogce et al. [26] have estimated that ~25% of colorectal, ~15% of breast and ~10% of prostate, pancreas and endometrial cancers could be reduced by shifting to a traditional healthy Mediterranean diet in developed Western countries. It is known that Western diets are rich in red and processed meat and poor in fruits and vegetables, and some studies have suggested that they can promote the occurrence of certain cancers (colon, prostate, endometrium and breast) [27] [28]. Similar to the Mediterranean diet, the Japanese dietary pattern, characterized by the low consumption of fatty acids and high consumption of rice, soy-derived proteins and fish, has also been associated with lower rates of prostate and breast cancer in Asians [29]. "
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    ABSTRACT: Currently, the main treatments available for cancer include surgery, biological therapy, radiation and chemotherapy. However, these treatments have strong secondary effects on patients, which can prohibit their use. Therefore, the search for alternative treatments is a current challenge for scientists. Several studies have identified compounds from plants that exhibit biological properties compatible with the desired activity of anti-neoplastic drugs. Natural products are thought to be more compatible with the human body and cause fewer side effects. Furthermore, substances present in fruits, vegetables and herbal essential oils have demonstrated important antiproliferative activity, inducing cell and genomic changes favorable for cancer prevention and therapy. Taking into account that the molecular mechanisms by which natural compounds function to prevent cancer are not fully understood and that molecular targets can be important tools for evaluating their effectiveness, this chapter aims to present and discuss potential active compounds as possible anti-cancer agents.
    Frontiers in Clinical Drug Research - Anti-Cancer Agents, 1 edited by Atta-ur-Rahman, 06/2015: chapter Some Natural Products May Represent a Future Alternative to Anti-Neoplastic Medicine: pages 209-229; Atta-ur-Rahman., ISBN: 978-1-68108-073-4
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    • "From a public health perspective, cigarette smoking is the single most important cause of human cancer. In high-income countries, tobacco smoking is responsible for 25 – 30% of overall cancer mortality [11]. Smoking is associated with elevated rates of cancer of the lung, bladder, cervix, colon and rectum, oesophagus, kidney, larynx, mouth and throat, pancreas, stomach, nasal cavity, liver, ovaries, and with acute myelogenous leukemia [12]. "
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    ABSTRACT: Background There is conflicting evidence regarding the associations between cigarette smoking and glioma or meningioma. Our purpose is to provide further evidence on these possible associations. Methods We conducted a set of case–control studies in three Canadian cities, Montreal, Ottawa and Vancouver. The study included 166 subjects with glioma, 93 subjects with meningioma, and 648 population-based controls. A lifetime history of cigarette smoking was collected and various smoking indices were computed. Multivariable logistic regression was used to estimate odds ratios (ORs) between smoking and each of the two types of brain tumours. Results Adjusted ORs between smoking and each type of brain tumour were not significantly elevated for all smokers combined or for smokers with over 15 pack-years ((packs / day) x years) accumulated. We tested for interactions between smoking and several sociodemographic variables; the interaction between smoking and education on glioma risk was significant, with smoking showing an elevated OR among subjects with lower education and an OR below unity among subjects with higher education. Conclusion Except for an unexplained and possibly artefactual excess risk in one population subgroup, we found little or no evidence of an association between smoking and either glioma or meningioma.
    Environmental Health 06/2014; 13(1):55. DOI:10.1186/1476-069X-13-55 · 3.37 Impact Factor
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    • "Generally, the morphology of the tumor cells, immunophenotype, genetic abnormalities and clinical features are used in classification (Weng et al., 2012). Although the etiology is largely unknown, several exogenous toxicants including cytotoxic drugs, benzene, ionizing radiation and tobacco smoking were described as causative factors (Descatha et al., 2005; Irigaray et al., 2007). Targeted disease association studies aiming to identify genetic factors leading to susceptibility to HM resulted in identification of several candidate genes but positive results generally have not been replicated in subsequent studies. "
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    ABSTRACT: Hematological malignancies (HM) are a group of neoplasms derived from the cells of the bone marrow and lymphatic system. Genetic factors leading to susceptibility to HM have been investigated for years but little is known yet. Low molecular weight polypeptide (LMP) 2 and LMP7 genes are important subunits of the immunoproteasome and play significant role in antigen presentation. The polymorphisms of LMP genes have been reported to be risk factors for various types of diseases. The aim of this study was to investigate the association of LMP2 and LMP7 polymorphisms with the occurrence of particular types of HM. A total of 132 patients with HM and 130 control subjects were investigated. No significant difference was obtained in the distribution of genotype and allele frequencies of LMP7 gene in HM patients and the control group. On the other hand, the prevalence of LMP2-AA genotype was found to be higher in acute myeolid leukemia (AML) patients while it was significantly lower in multiple myeloma (MM) cases than in the control subjects. Our results suggested that LMP7 could not be a risk factor for susceptibility to HM, whereas LMP2 polymorphisms could play a role in the development of AML and MM.
    Asian Pacific journal of cancer prevention: APJCP 11/2013; 14(11):6399-402. DOI:10.7314/APJCP.2013.14.11.6399 · 2.51 Impact Factor
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