Histopathological data of iron and calcium in the mouse lung after asbestos exposure

Trevisan, Elisa; Zabucchi, Giuliano; Pascolo, Lorella; Pascotto, Ernesto; Casarsa, Claudia; Lucattelli, Monica; Lungarella, Giuseppe; Cavarra, Eleonora; Bartalesi, Barbara; Zweyer, Marina; Borelli, Violetta

doi:10.1016/j.dib.2016.01.026

Cited by 4 publications

(3 citation statements)

References 5 publications

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“…In vivo and in vitro studies demonstrated that both chrysotile and crocidolite induce oxidative stress and the production of local inflammatory mediators such as cytokines and growth factors. This leads to a reactive microenvironment characterized by inflammation and proliferation of mesothelial cells ultimately inducing MPM or other asbestos-related diseases (Nymark et al 2007;Trevisan et al 2016). Mesothelial cells exposed to crocidolite were reported to have an extensive altered expression of genes involved in integrin-mediated signalling pathways, DNA damage repair, and cell cycle regulation (Acencio et al 2015;Wang et al 2011).…”

Section: Introductionmentioning

confidence: 99%

DNA methylation profiling of asbestos-treated MeT5A cell line reveals novel pathways implicated in asbestos response

et al. 2018

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Occupational and environmental asbestos exposure is the main determinant of malignant pleural mesothelioma (MPM), however, the mechanisms by which its fibres contribute to cell toxicity and transformation are not completely clear. Aberrant DNA methylation is a common event in cancer but epigenetic modifications involved specifically in MPM carcinogenesis need to be better clarified. To investigate asbestos-induced DNA methylation and gene expression changes, we treated Met5A mesothelial cells with different concentrations of crocidolite and chrysotile asbestos (0.5 ÷ 5.0 µg/cm, 72 h incubation). Overall, we observed 243 and 302 differentially methylated CpGs (≥ 10%) between the asbestos dose at 5 µg/cm and untreated control, in chrysotile and crocidolite treatment, respectively. To examine the dose-response effect, Spearman's correlation test was performed and significant CpGs located in genes involved in migration/cell adhesion processes were identified in both treatments. Moreover, we found that both crocidolite and chrysotile exposure induced a significant up-regulation of CA9 and SRGN (log2 fold change > 1.5), previously reported as associated with a more aggressive MPM phenotype. However, we found no correlation between methylation and gene expression changes, except for a moderate significant inverse correlation at the promoter region of DKK1 (Spearman rho = - 1, P value = 0.02) after chrysotile exposure. These results describe for the first time the relationship between DNA methylation modifications and asbestos exposure. Our findings provide a basis to further explore and validate asbestos-induced DNA methylation changes, that could influence MPM carcinogenesis and possibly identifying new chemopreventive target.

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Section: Introductionmentioning

confidence: 99%

DNA methylation profiling of asbestos-treated MeT5A cell line reveals novel pathways implicated in asbestos response

et al. 2018

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“…40 Chrysotile and crocidolite types of asbestos were shown to induce oxidative stress and induce local inflammatory mediators (cytokines and growth factors), leading to a reactive microenvironment of inflammation and proliferation of cells. 41,42 Exposure of cells to asbestos induces extensive alterations in expression of genes involved in integrinmediated signalling, DNA damage repair, and cell cycle regulation pathways. 43,44 The chronic inflammation caused by exposure of serosal surfaces to asbestos fibres is likely to represent a central factor in the carcinogenesis and is likely to be mediated through epigenetic changes.…”

Section: Asbestos-induced Epigenetic Changes (Figure 1)mentioning

confidence: 99%

<p>The Current Understanding Of Asbestos-Induced Epigenetic Changes Associated With Lung Cancer</p>

Cheng¹,

Rath²,

Linton³

et al. 2020

LCTT

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Asbestos is a naturally occurring mineral consisting of extremely fine fibres that can become trapped in the lungs after inhalation. Occupational and environmental exposures to asbestos are linked to development of lung cancer and malignant mesothelioma, a cancer of the lining surrounding the lung. This review discusses the factors that are making asbestos-induced lung cancer a continuing problem, including the extensive historic use of asbestos and decades long latency between exposure and disease development. Genomic mutations of DNA nucleotides and gene rearrangements driving lung cancer are well-studied, with biomarkers and targeted therapies already in clinical use for some of these mutations. The genes involved in these mutation biomarkers and targeted therapies are also involved in epigenetic mechanisms and are discussed in this review as it is hoped that identification of epigenetic aberrations in these genes will enable the same gene biomarkers and targeted therapies to be used. Currently, understanding of how asbestos fibres trapped in the lungs leads to epigenetic changes and lung cancer is incomplete. It has been shown that oxidoreduction reactions on fibre surfaces generate reactive oxygen species (ROS) which in turn damage DNA, leading to genetic and epigenetic alterations that reduce the activity of tumour suppressor genes. Epigenetic DNA methylation changes associated with lung cancer are summarised in this review, and some of these changes will be due to asbestos exposure. So far, little research has been carried out to separate the asbestos driven epigenetic changes from those due to non-asbestos causes of lung cancer. Asbestos-associated lung cancers exhibit less methylation variability than lung cancers in general, and in a large proportion of samples variability has been found to be restricted to promoter regions. Epigenetic aberrations in cancer are proving to be promising biomarkers for diagnosing cancers. It is hoped that further understanding of epigenetic changes in lung cancer can result in useful asbestos-associated lung cancer biomarkers to guide treatment. Research is ongoing into the detection of lung cancer epigenetic alterations using non-invasive samples of blood and sputum. These efforts hold the promise of non-invasive cancer diagnosis in the future. Efforts to reverse epigenetic aberrations in lung cancer by epigenetic therapies are ongoing but have not yet yielded success.

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“…Previously, cytotoxic effects of asbestos fibres have been investigated both in in vitro cellular models (Casalone et al, 2018), as well as in animal models (Altomare et al, 2005;Trevisan et al, 2016), with reports present from as early as 1970s (Davis, Bolton, & Garrett, 1974). Most studies have investigated the relationship between asbestos exposure, cytotoxicity, and asbestos-induced cellular and molecular alterations on human or animal derived mesothelial cells (Casalone et al, 2018;Kopnin et al, 2004), lung fibroblasts , or macrophages (Nadeau & Lane, 1988).…”

Section: Introduction To the Chaptermentioning

confidence: 99%

A multimodal approach to identify asbestos and characterise clinically relevant mesothelioma biomarkers

Voloacă¹

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Malignant mesothelioma (MM) is an aggressive cancer of the mesothelium, with long latency and poor overall survival (OS), associated with occupational and environmental exposure to asbestos and other mineral fibres (MF). Considering that early diagnosis has been linked to an improvement in prognosis and treatment response, there is an urgent need for reliable MM biomarkers. Additionally, current asbestos identification techniques lack sensitivity and fail to detect shorter fibres or fibre fragments. Accurately identifying MF within MM samples is not only essential in aiding early diagnosis, but it also plays a key role in linking this diagnosis to asbestos exposure, which has high implications in legal, social, and political matters. The aim of the current project is to (1) develop MM cellular models suitable for laser ablation inductively coupled plasma mass spectrometry (LA-ICP-MS) imaging, (2) identify various MF based on their metal content within MM in vitro models as well as patient samples using a combination of LA-ICP-MS and LA-ICP-time of flight (TOF)MS instrumentation, (3) investigate the MM metallome in human tissue samples using LA-ICP-MS elemental mapping, and (4) characterise a panel of emerging MM biomarkers using a multi-modal approach. For the first time, this study has developed an asbestos detection technique using LA-ICP-MS imaging to identify MF within MM samples. High-resolution and high-speed analysis suggests that LA-ICP-MS imaging has the potential to be ultimately integrated in the clinical workflow to aid the identification of patients at an earlier and more treatable stage to improve survival outcomes. Moreover, the selected panel of biomarkers was characterised in cellular models, whilst novel biomarkers were tentatively identified using matrix assisted laser desorption ionisation (MALDI)-MS imaging of tissue microarrays, setting the basis for vital future investigations, and ultimately supporting MM biomarker discovery, early diagnosis, and improved prognosis.

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Histopathological data of iron and calcium in the mouse lung after asbestos exposure

Cited by 4 publications

References 5 publications

DNA methylation profiling of asbestos-treated MeT5A cell line reveals novel pathways implicated in asbestos response

DNA methylation profiling of asbestos-treated MeT5A cell line reveals novel pathways implicated in asbestos response

<p>The Current Understanding Of Asbestos-Induced Epigenetic Changes Associated With Lung Cancer</p>

A multimodal approach to identify asbestos and characterise clinically relevant mesothelioma biomarkers

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