Lamia Benbrahim‐Tallaa

Centre International de Recherche sur le Cancer

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Fatiha El Ghissassi

Centre International de Recherche sur le Cancer

Yann Grosse

Centre International de Recherche sur le Cancer

Véronique Bouvard

Centre International de Recherche sur le Cancer

Kurt Straíf

Barcelona Institute for Global Health

Neela Guha

California Environmental Protection Agency

Béatrice Secretan

Centre International de Recherche sur le Cancer

Heidi Mattock

Centre International de Recherche sur le Cancer

Robert A. Baan

Centre International de Recherche sur le Cancer

Kathryn Z. Guyton

National Academies of Sciences, Engineering, and Medicine

Dana Loomis

University of Nevada, Reno

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Centre International de Recherche sur le Cancer

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National Cancer Institute

National Institutes of Health

Inserm

National Institute of Environmental Health Sciences

Division of Cancer Epidemiology and Genetics

Harvard University

Research Triangle Park Foundation

Brigham and Women's Hospital

University of North Carolina at Chapel Hill

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Cancer in experimental animals exposed to arsenic and arsenic compounds

Critical Reviews in Toxicology (2010)

Erik J. Tokar Lamia Benbrahim‐Tallaa Jerrold M. Ward Ruth M. Lunn Reeder Sams

Inorganic arsenic is a ubiquitous environmental contaminant that has long been considered a human carcinogen. Recent studies raise further concern about the metalloid as a major, naturally occurring carcinogen in the environment. However, during this same period it has proven difficult to provide experimental evidence of the carcinogenicity of inorganic arsenic in laboratory animals and, until recently, there was considered to be a lack of clear evidence for carcinogenicity of any arsenical in animals. More recent work with arsenical methylation metabolites and early life exposures to inorganic arsenic has now provided evidence of carcinogenicity in rodents. Given that tens of millions of people worldwide are exposed to potentially unhealthy levels of environmental arsenic, in vivo rodent models of arsenic carcinogenesis are a clear necessity for resolving critical issues, such as mechanisms of action, target tissue specificity, and sensitive subpopulations, and in developing strategies to reduce cancers in exposed human populations. This work reviews the available rodent studies considered relevant to carcinogenic assessment of arsenicals, taking advantage of the most recent review by the International Agency for Research on Cancer (IARC) that has not yet appeared as a full monograph but has been summarized (IARC, 2009 , IARC Special Report: Policy, Vol. 10. Lyon: IARC Press, 453–454). Many valid studies show that arsenic can interact with other carcinogens/agents to enhance oncogenesis, and help elucidate mechanisms, and these too are summarized in this review. Finally, this body of rodent work is discussed in light of its impact on mechanisms and in the context of the persistent argument that arsenic is not carcinogenic in animals.

International agency

Arsenic toxicity

10.3109/10408444.2010.506641

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Citations (125)

Carcinogenicity of chemicals in industrial and consumer products, food contaminants and flavourings, and water chlorination byproducts

The Lancet Oncology (2011)

Yann Grosse Robert A. Baan Béatrice Secretan Fatiha El Ghissassi Véronique Bouvard

10.1016/s1470-2045(11)70088-2

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Acquisition of Androgen Independence by Human Prostate Epithelial Cells during Arsenic-Induced Malignant Transformation

Environmental Health Perspectives (2005)

Lamia Benbrahim‐Tallaa Mukta M. Webber Michael P. Waalkes

Lethal phenotypes of human prostate cancer are characterized by progression to androgen independence, although the mechanisms behind this progression remain unclear. Arsenic is a potential human prostate carcinogen that may affect tumor progression. In this study, we used a prostate cancer cell model in which an immortalized, nontumorigenic human prostate epithelial cell line (RWPE-1) had been malignantly transformed by chronic low-level arsenic to help determine whether arsenic affects prostate tumor progression. Control and CAsE-PE (chronic-arsenic-exposed human prostate epithelial) cells were continuously maintained in a complete medium [keratinocyte serum-free medium (K-SFM) with bovine pituitary extract and epidermal growth factor] or in a steroid-depleted medium (K-SFM alone). The arsenic-transformed cells showed a more rapid proliferation rate in complete medium than did control cells and also showed sustained proliferation in steroid-reduced medium. Although both control and CAsE-PE cells showed similar levels of androgen receptor (AR), androgens were less effective in stimulating cell proliferation and AR-related gene expression in CAsE-PE cells. For instance, dihydrotestosterone caused a 4.5-fold increase in prostate-specific antigen transcript in control cells but only a 1.5-fold increase in CAsE-PE cells. CAsE-PE cells also showed relatively low levels of growth stimulation by nonandrogen steroids, such as estradiol. Thus, arsenic-induced malignant transformation is associated with acquired androgen independence in human prostate cells. This acquired androgen independence was apparently not due to AR up-regulation, increased activity, or altered ligand specificity. The precise manner in which arsenic altered CAsE-PE growth and progression is undefined but may involve a bypass of AR involving direct stimulation of downstream signaling pathways.

Dihydrotestosterone

Malignant Transformation

10.1289/ehp.7832

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Citations (35)

Future priorities for the IARC Monographs

The Lancet Oncology (2014)

Kurt Straíf Dana Loomis Kathryn Z. Guyton Yann Grosse Béatrice Secretan

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Advisory committee

10.1016/s1470-2045(14)70168-8

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O-095 MECHANISMS OF CARCINOGENICITY OF OCCUPATIONAL EXPOSURES: INTEGRATION OF THE MECHANISTIC EVIDENCE IN THE IARC MONOGRAPHS OVERALL EVALUATION IN THE LAST 10 YEARS

Occupational Medicine (2024)

Fatiha El Ghissassi Lamia Benbrahim‐Tallaa Aline de Conti Federica Madia

Abstract Introduction Over the years, mechanistic data has become critical to the understanding of human cancer hazards. Their increasing prominence was reflected in the 2019 revision of the IARC Monographs Preamble, which has placed mechanistic evidence, through the application of the key characteristics (KCs) of human carcinogens, alongside evidence for cancer in humans and experimental animals in the integration of evidence. Here, the evolution on the use of this information is described in the evaluation of occupational exposures. Methods Occupational exposures such as, styrene/styrene oxide, night shift work, 1,1,1-Trichloroethane, and recently occupational exposure as a firefighter and 2-bromopropane were examined based on the available studies, strength of the various KCs, and relevance of the associated endpoints across test systems. Results The evidence, as described by the 10 KCs, was supportive or strong and contributed substantially to the description of the mechanisms and the overall evaluation when the evidence from epidemiological studies was sufficient (for firefighting exposure), mainly limited or inadequate (for styrene oxide and 2-bromopropane), and it was sufficient for cancers in animal studies. Discussion Several KCs such as it is genotoxic, induces chronic inflammation and modulates receptor mediated effects or is immunosuppressive, for which the evaluation of mechanistic studies was consistent and coherent contributed to the overall evaluation of the occupational agents as IARC group 1 or Group 2A. Conclusion Mechanistic information is critical to the identification of carcinogenic hazard the KCs are a powerful tool that allow understanding further the mechanisms contributing to the carcinogenicity.

10.1093/occmed/kqae023.0687

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Use of mechanistic data in the IARC evaluations of the carcinogenicity of polychlorinated biphenyls and related compounds

Environmental Science and Pollution Research (2015)

Béatrice Secretan Dana Loomis Robert A. Baan Fatiha El Ghissassi Véronique Bouvard

Polybrominated Biphenyls

10.1007/s11356-015-4829-4

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Citations (58)

Carcinogenicity of diesel- (DEE) and gasoline-engine exhausts (GEE)

Toxicology Letters (2014)