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doi:10.1002/ijc.v141.10

Cited by 10 publications

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“…44 The relationship between promoter DNA hypermethylation and inflammation has been documented in many forms of cancer, including asbestosrelated lung cancer. 76 It is hypothesised that asbestos exposure contributes to lung cancer formation through this relationship. 45 Genomic investigations have shown DNA copy number alterations, changes in miRNA profiles, and deregulation of expression of certain genes in asbestos-related lung cancer.…”

Section: Dna Methylation In Lung Cancersmentioning

confidence: 99%

“…Cheng et al Lung cancer cases with no documented occupational exposure to asbestos have been found to have larger methylation variability and a higher proportion of hypomethylated DVMCs than asbestos-exposed subjects. 76 A large proportion of DVMCs in lung tumours of the asbestos-exposed subjects have been found within 1 kilobasepair (kb) of promoter regions. 76 The genes NPTN, NRG2, and TRPC3 exhibit significant asbestosrelated DVMCs.…”

Section: Dovepressmentioning

confidence: 99%

“…76 A large proportion of DVMCs in lung tumours of the asbestos-exposed subjects have been found within 1 kilobasepair (kb) of promoter regions. 76 The genes NPTN, NRG2, and TRPC3 exhibit significant asbestosrelated DVMCs. 76 NRG2 has a cell proliferation role and thus its DVMC in asbestos-related lung cancers may be playing a role in the cancer.…”

Section: Dovepressmentioning

confidence: 99%

“…76 The genes NPTN, NRG2, and TRPC3 exhibit significant asbestosrelated DVMCs. 76 NRG2 has a cell proliferation role and thus its DVMC in asbestos-related lung cancers may be playing a role in the cancer. 76 Little is known about the role of NPTN (neuroplastin), and it may potentially be involved in modulating intracellular Ca 2+ as a result of its interaction with FGFR.…”

Section: Dovepressmentioning

confidence: 99%

“…76 NRG2 has a cell proliferation role and thus its DVMC in asbestos-related lung cancers may be playing a role in the cancer. 76 Little is known about the role of NPTN (neuroplastin), and it may potentially be involved in modulating intracellular Ca 2+ as a result of its interaction with FGFR. 79 This may result in stimulating the Ca 2+ sensing receptor that promotes the expression of TRPC3, a member of the canonical transient receptor potential channels, leading to perturbation in Ca 2+ homeostasis.…”

Section: Dovepressmentioning

confidence: 99%

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<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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Section: Dna Methylation In Lung Cancersmentioning

confidence: 99%

Section: Dovepressmentioning

confidence: 99%

Section: Dovepressmentioning

confidence: 99%

Section: Dovepressmentioning

confidence: 99%

Section: Dovepressmentioning

confidence: 99%

See 3 more Smart Citations

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

Cheng¹,

Rath²,

Linton³

et al. 2020

LCTT

View full text Add to dashboard Cite

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Use of Big Data to Estimate Prevalence of Defective DNA Repair Variants in the US Population

et al. 2019

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IMPORTANCE Wide use of genomic sequencing to diagnose disease has raised concern about the extent of genotype-phenotype correlations.OBJECTIVE To correlate disease-associated allele frequencies with expected and reported prevalence of clinical disease. DESIGN, SETTING, AND PARTICIPANTS Xeroderma pigmentosum (XP), a recessive, cancer-prone, neurocutaneous disorder, was used as a model for this study. From January 1, 2017, to May 4, 2018, the Human Gene Mutation Database and a cohort of patients at the National Institutes of Health were searched and screened to identify reported mutations associated with XP. The clinical phenotype of these patients was confirmed from reports in the literature and National Institutes of Health medical records. The genetically predicted prevalence of disease based on frequency of known pathogenic mutations was compared with the prevalence of patients clinically diagnosed with phenotypic XP. Exome sequencing of more than 200 000 alleles from the Genome Aggregation Database, the National Cancer Institute Division of Cancer Epidemiology and Genetics database of healthy controls, and an Inova Hospital Study database was used to investigate the frequencies of these mutations in the general population. MAIN OUTCOMES AND MEASURESListing of all reported mutations associated with XP, their frequencies in 3 large exome sequence databases, determination of the number of patients in the United States with XP using modeling equations, and comparison of the observed and reported numbers of patients with XP with specific mutations.RESULTS A total of 156 pathogenic missense and nonsense mutations associated with XP were identified in the National Institutes of Health cohort and the Human Gene Mutation Database. The Genome Aggregation Database provided frequency data for 65 of these mutations, with a total allele frequency of 1.13%. The XPF (ERCC4) mutation, p.P379S, had an allele frequency of 0.4%, and the XPC mutation, p.P334H, had an allele frequency of 0.3%. With the Hardy-Weinberg equation, it was determined that there should be more than 8000 patients who are homozygous for these mutations in the United States. In contrast, only 3 patients with XP were reported as having the XPF mutation, and 1 patient was reported as having the XPC mutation. CONCLUSIONS AND RELEVANCEThe findings from this study suggest that clinicians should approach large genomic databases with caution when trying to correlate the clinical implications of genetic variants with the prevalence of disease risk. Unsuspected mutations in known genes with a predisposition for skin cancer may be responsible for some of the high frequency of skin cancers in the general population.

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Survival Rates for Patients With Barrett High-grade Dysplasia and Esophageal Adenocarcinoma With or Without Human Papillomavirus Infection

et al. 2018

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Key Points Question What is the prognostic significance of esophageal tumor human papillomavirus (HPV) status? Findings In this case-control study involving 142 patients with Barrett high-grade dysplasia and esophageal adenocarcinoma, HPV positivity was associated with a significantly improved disease-free survival compared with viral negativity. Recurrence and progression were reduced in the HPV-positive cohort as were distant metastasis and death from esophageal adenocarcinoma. Meaning Barrett high-grade dysplasia and esophageal adenocarcinoma in patients who are HPV positive have a favorable prognosis compared with viral-negative esophageal tumors and may benefit from treatment de-escalation.

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Untitled

Cited by 10 publications

References 0 publications

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

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

Use of Big Data to Estimate Prevalence of Defective DNA Repair Variants in the US Population

Survival Rates for Patients With Barrett High-grade Dysplasia and Esophageal Adenocarcinoma With or Without Human Papillomavirus Infection

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