scholarly journals Environmental carcinogen control in Australia: the need for a strategy

2002 ◽  
Vol 13 (10) ◽  
pp. 199
Author(s):  
Andrew Penman
Keyword(s):  
Environmental Carcinogen ◽  
Carcinogen Control

Metabolism and mutagenicity of dibenzo[a,e]pyrene and the very potent environmental carcinogen dibenzo[a,l]pyrene

1990 ◽  
Vol 3 (6) ◽  
pp. 580-586 ◽  
Author(s):  
Prabhakar D. Devanesan ◽  
Paolo Cremonesi ◽  
Janet E. Nunnally ◽  
Eleanor G. Rogan ◽  
Ercole L. Cavalieri
Keyword(s):  
Environmental Carcinogen

scholarly journals Applying a Weight-of-Evidence Approach to Evaluate Relevance of Molecular Landscapes in the Exposure-Disease Paradigm

2015 ◽  
Vol 2015 ◽  
pp. 1-11
Author(s):  
Sherilyn A. Gross ◽  
Kristen M. Fedak
Keyword(s):  
Molecular Mechanisms ◽  
Molecular Data ◽  
Weight Of Evidence ◽  
Molecular Characteristics ◽  
Environmental Carcinogens ◽  
Environmental Carcinogen ◽  
Cell Counts ◽  
Disease Outcomes ◽  
Dna Repair Gene ◽  
Increased Risk

Information on polymorphisms, mutations, and epigenetic events has become increasingly important in our understanding of molecular mechanisms associated with exposures-disease outcomes. Molecular landscapes can be developed to illustrate the molecular characteristics for environmental carcinogens as well as associated disease outcomes, although comparison of these molecular landscapes can often be difficult to navigate. We developed a method to organize these molecular data that uses a weight-of-evidence approach to rank overlapping molecular events by relative importance for susceptibility to an exposure-disease paradigm. To illustrate the usefulness of this approach, we discuss the example of benzene as an environmental carcinogen and myelodysplastic syndrome (MDS) as a causative disease endpoint. Using this weight-of-evidence method, we found overlapping polymorphisms in the genes for the metabolic enzymesGSTandNQO1, both of which may infer risk of benzene-induced MDS. Polymorphisms in the tumor suppressor gene,TP53, and the inflammatory cytokine gene,TNF-α, were also noted, albeit inferring opposing outcomes. The alleles identified in the DNA repair geneRAD51indicated an increased risk for MDS in MDS patients and low blood cell counts in benzene-exposed workers. We propose the weight-of-evidence approach as a tool to assist in organizing the sea of emerging molecular data in exposure-disease paradigms.

scholarly journals TP53 Mutational signature for aristolochic acid: an environmental carcinogen

2011 ◽  
Vol 129 (6) ◽  
pp. 1532-1536 ◽  
Author(s):  
Masaaki Moriya ◽  
Neda Slade ◽  
Branko Brdar ◽  
Zvonimir Medverec ◽  
Karla Tomic ◽  
...  
Keyword(s):  
Aristolochic Acid ◽  
Environmental Carcinogen ◽  
Mutational Signature

scholarly journals How the AHR Became Important in Cancer: The Role of Chronically Active AHR in Cancer Aggression

2020 ◽  
Vol 22 (1) ◽  
pp. 387
Author(s):  
Zhongyan Wang ◽  
Megan Snyder ◽  
Jessica E. Kenison ◽  
Kangkang Yang ◽  
Brian Lara ◽  
...  
Keyword(s):  
Malignant Cell ◽  
Unintended Consequences ◽  
Chemical Toxicity ◽  
Environmental Chemical ◽  
Environmental Carcinogen ◽  
Aryl Hydrocarbon ◽  
Cell Progression ◽  
Human Pollution ◽  
Normal Physiological Function

For decades, the aryl hydrocarbon receptor (AHR) was studied for its role in environmental chemical toxicity i.e., as a quirk of nature and a mediator of unintended consequences of human pollution. During that period, it was not certain that the AHR had a “normal” physiological function. However, the ongoing accumulation of data from an ever-expanding variety of studies on cancer, cancer immunity, autoimmunity, organ development, and other areas bears witness to a staggering array of AHR-controlled normal and pathological activities. The objective of this review is to discuss how the AHR has gone from a likely contributor to genotoxic environmental carcinogen-induced cancer to a master regulator of malignant cell progression and cancer aggression. Particular focus is placed on the association between AHR activity and poor cancer outcomes, feedback loops that control chronic AHR activity in cancer, and the role of chronically active AHR in driving cancer cell invasion, migration, cancer stem cell characteristics, and survival.

CAREX CANADA: OCCUPATIONAL AND ENVIRONMENTAL CARCINOGEN SURVEILLANCE

2011 ◽  
Vol 2011 (1) ◽  
Author(s):  
Paul A Demers ◽  
Eleanor S Setton ◽  
Cheryl E Peters ◽  
Perry Hystad ◽  
Amy L Hall ◽  
...  
Keyword(s):  
Environmental Carcinogen
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