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Volume 36, Issue Suppl_1
June 2015
ISSN 0143-3334
EISSN 1460-2180
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Assessing the Carcinogenic Potential of Low-Dose Exposures to Chemical Mixtures in the Environment: The Challenge Ahead

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Editorial

Review

This review of environmental chemical carcinogenesis is focused on the immune evasion mechanisms. It is important to know whether or not certain ubiquitous in anthropogenic environment chemicals interfere with host immune response, thus augmenting the risk of cancer cell survival.

In this review, we discuss how environmental exposures can perturb the tumor microenvironment, a complex network comprised of fibroblasts, epithelial cells, stroma, extracellular matrix and immune cells, and contribute to multiple stages of tumor growth.

Angiogenesis is an important ‘hallmark’ of cancer. We reviewed the various pathways controlling angiogenesis, summarized the possible role of specific environmental chemicals disrupting these pathways and listed assays for assessing the effects of low-dose exposures to chemicals in promoting tumor angiogenesis.

There is an urgent need to understand the molecular mechanisms by which sustained exposure to low-dose environmental chemical mixtures promotes carcinogenesis. This Halifax Project review specifically examines the effects of environmental chemicals on the cancer hallmark of evading growth suppression.

Dysregulated metabolism represents one of the most common and recognizable features of cancer. Specific roles for metabolic reprogramming in environmental carcinogenesis, however, remain incompletely delineated. The present review addresses corresponding knowledge gaps and the limitations of current experimental approaches to the problem.

Exposure to common environmental chemicals at low doses and in mixtures that act as immune disruptors and destabilize the balance of pro- and anti-inflammatory responses in favor of inflammation may increase cancer risk in exposed individuals. This risk and the potential for transgenerational inheritance through epigenetic effects to offspring are understudied in the cancer field and overlooked by current toxicant screening platforms for carcinogenesis.

Low-dose exposures to common environmental chemicals that are deemed safe individually may be combining to instigate carcinogenesis, thereby contributing to the incidence of cancer. This risk may be overlooked by current regulatory practices and needs to be vigorously investigated.

In this review, we focus on some ‘chemical disruptors’ and how they add to the burden of genome instability, thereby increasing cancer incidence risk.

Chemical carcinogenesis is caused mainly by the modulation of important cellular mechanisms and pathways that regulate cell death. Mechanisms of several environmental chemicals that disrupt these important targets conferring resistance to cell death have been discussed.

Dedication

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