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Global Burden and Aspects of Occupational Cancer
Published in Thomas P. Fuller, Global Occupational Safety and Health Management Handbook, 2019
In order to replace the use of animal studies, new toxicokinetic and mechanistic studies are expanding drastically. These methods use what is already known about the mutational signatures that comprise tumors and cancer cells and compare them with other similar chemicals that would be expected or likely to result in similar outcomes. It becomes a systematic method to evaluate mechanistic data and identify likely toxicological outcomes for various chemicals by comparing them to the biological outcomes of other known carcinogens. Some of the mechanistic signals of carcinogenesis have included such characteristics as transformation of metabolites that can damage DNA, alteration of gene expression, disruption of the immune system, and interference with molecular communication. Results of these types of studies, combined with sophisticated mathematical and computational manipulations, can lead to the evaluation of significantly more potential carcinogens in much less time than previously possible. Future advances in these types of studies will continually expand to include toxicological predictions based on physical and chemical properties of molecules, genomic responses of biological samples, cancer pathway and network analyses, and even clinical studies of molecular changes in tissues of exposed humans (Cote, 2016; NTP, 1999; EPA, 2017).
A pilot study of exome sequencing in a diverse New Zealand cohort with undiagnosed disorders and cancer
Published in Journal of the Royal Society of New Zealand, 2018
Colina McKeown, Samantha Connors, Rachel Stapleton, Tim Morgan, Ian Hayes, Katherine Neas, Joanne Dixon, Kate Gibson, David M. Markie, Peter Tsai, Cherie Blenkiron, Sandra Fitzgerald, Paula Shields, Patrick Yap, Ben Lawrence, Cristin Print, Stephen P. Robertson
It seems likely that precision oncology will require more than simple WES. For example, solid tumours are frequently heterogeneous, requiring DTS to identify sub-clonal mutations (Patel & Tsui 2015; Morris et al. 2016). Mutational signatures are also emerging as an important indicator of tumour biology and patient 13 may have benefited from additional whole genome sequencing to identify these signatures (Morris et al. 2016). Knowing whether the BRCA1- and EP300-mutant tumour of this patient had the pan-genome DNA repair defect associated with BRCA pathway failure would give more certainty to clinical decisions about the use of platinum drugs or poly ADP ribose polymerase (PARP) inhibitors (Alexandrov et al. 2013). Sequencing of circulating tumour DNA facilitates quantification of tumour heterogeneity and detection of mutations in small, surgically inaccessible or radiologically invisible tumours (Patel & Tsui 2015). Finally, RNA expression analysis could identify potential BRCA1 haploinsufficiency and the effects of extensive LoH on oncogenic pathways (Sedic et al. 2015; Durrbaum & Storchova 2016).