Frontiers in Genetics

Our medical research library holds 13 studies published in Frontiers in Genetics (2011–2026). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 12 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it.

About the journal

• Publisher: Frontiers Research Foundation
• Published: 2010 to the present, Switzerland
• Language: English
• ISSN: 1664-8021 (electronic)
• Its record in the NLM Catalog

2020s

• FANCD2 knockdown suppresses malignant phenotypes and is associated with caspase/PARP-mediated apoptosis in NCI-H2052 pleural mesothelioma cells. Y. Xiang, P. Su, R. Zhang, et al. 2026;17:1926600. PubMed · Publisher · Free full text

  Abstract

  Background: Malignant pleural mesothelioma (PM) is a highly aggressive thoracic malignancy with an extremely poor prognosis and limited effective therapeutic strategies, representing a critical unmet clinical need. Fanconi anemia complementation group D2 (FANCD2) is a critical effector of the cellular DNA damage response system and plays a central role in maintaining genomic integrity. While the genoprotective functions of FANCD2 have been extensively characterized, its specific biological roles and molecular regulatory mechanisms in the malignant progression of PM remain poorly understood. The current study aimed to evaluate FANCD2 expression and its clinical associations in PM and to examine the effects of transient FANCD2 knockdown in NCI-H2052 cells.

  Methods: Comprehensive bioinformatics analyses were performed based on public transcriptomic data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases to profile FANCD2 expression patterns and evaluate its clinical prognostic value in PM. Differential expression analysis was applied to confirm the aberrant upregulation of FANCD2 in PM tissues, and the associations of FANCD2 expression levels with tumor pathological staging and patient clinical prognosis were systematically assessed. Western blotting was further performed to evaluate the protein expression status of FANCD2 in clinical PM specimens and NCI-H2052 cells, with normal tissues and corresponding normal cells included as control groups. Transient FANCD2 knockdown was achieved in NCI-H2052 cells using two independent small interfering RNAs (siRNAs). A series of functional experiments were conducted to determine the effects of FANCD2 silencing on the proliferation, wound closure, and apoptosis of NCI-H2052 cells. For mechanistic exploration, the expression levels of core apoptotic proteins were detected to evaluate the association between FANCD2 depletion and Caspase/PARP-related apoptotic signaling. In addition, tumor immune infiltration analysis was performed to investigate the correlation between FANCD2 expression and M2 macrophage infiltration within the PM tumor microenvironment (TME). FANCD2 rescue and Z-VAD-FMK inhibition experiments were performed to further evaluate the involvement of caspase-dependent apoptosis.

  Results: Bioinformatics results demonstrated that FANCD2 was significantly upregulated in PM tissues relative to normal control samples. Higher FANCD2 expression was associated with tumor T stage and unfavorable survival outcomes in the exploratory TCGA-MESO analysis. Consistently, Western blotting confirmed markedly increased FANCD2 protein levels in both clinical PM tissues and NCI-H2052 cells. Functional assays in NCI-H2052 cells revealed that siRNA-mediated FANCD2 knockdown significantly suppressed cell proliferation and reduced wound-closure capacity of NCI-H2052 cells, whereas it significantly increased apoptosis. Mechanistic investigations further found that FANCD2 silencing was associated with increased levels of caspase/PARP-related apoptotic markers, as evidenced by the markedly enhanced protein levels of cleaved caspase-3, cleaved caspase-8, cleaved caspase-9, and cleaved PARP. FANCD2 restoration and pharmacological caspase inhibition partially reversed FANCD2 knockdown-induced growth suppression and apoptosis, further supporting the involvement of caspase-dependent apoptotic signaling. Moreover, TME immune correlation analysis indicated that high FANCD2 expression was positively associated with M2 macrophage infiltration in PM tumors. These findings represent exploratory correlations derived from computational immune-cell estimation.

  Conclusion: In summary, FANCD2 may contribute to PM progression by supporting malignant phenotypes and limiting apoptosis. FANCD2 restoration and caspase inhibition partially reversed the growth suppression and apoptosis induced by FANCD2 knockdown, supporting the involvement of caspase-dependent apoptotic signaling. In addition, FANCD2 expression was positively associated with the computationally estimated proportion of M2 macrophages, suggesting that FANCD2 may represent an exploratory prognostic marker and a candidate therapeutic target for further investigation in PM.

  Copyright © 2026 Xiang, Su, Zhang, Zhao, Li, Yang, Lei, Chen, Zhang and Xiong.

• Machine learning, molecular docking, and experimental validation identify shared molecular signatures between idiopathic pulmonary arterial hypertension and malignant pleural mesothelioma: a retrospective study. N. Zhang, C. Wang, R. Wang, et al. 2026;17:1894027. PubMed · Publisher · Free full text

  Abstract

  Background: Idiopathic pulmonary arterial hypertension (IPAH) exhibits cancer-like features, yet its pathogenesis remains unclear. Given molecular similarities between IPAH and malignant pleural mesothelioma (MPM), this study aimed to uncover shared transcriptomic patterns.

  Methods: GEO datasets for IPAH and MPM were analyzed. Overlapping DEGs and WGCNA modules were identified. PPI network analysis combined with LASSO, random forest, and SVM-RFE was used to identify candidate biomarker genes. A classification model was constructed and evaluated using leave-one-out cross-validation and bootstrap optimism correction. Immune infiltration was evaluated by ssGSEA. Molecular docking and MD simulations assessed drug binding to candidate target proteins. qRT-PCR validated candidate biomarker gene expression.

  Results: Six concordantly upregulated and eleven concordantly downregulated DEGs were shared between IPAH and MPM. Upregulated genes were enriched in cell cycle regulation, while downregulated genes were enriched in neutrophil chemotaxis. WGCNA identified 58 overlapping genes. CXCR2, S100A9, and LCN2 were identified as candidate biomarker genes. A ROTS sensitivity analysis confirmed that all 1710 MPM DEGs were reproducible and directionally concordant at the matching FDR <0.05 threshold despite the imbalanced case-control ratio. The classification model achieved AUCs of 0.909 and 0.875 in training and external validation sets, with a LOOCV AUC of 0.879 and an optimism-corrected AUC of 0.896. Immune infiltration revealed increased Th17 cells but decreased neutrophils in IPAH. CXCR2 and S100A9 expression correlated with neutrophil infiltration; LCN2 expression correlated with metabolic reprogramming. Navarixin showed the strongest binding affinity to CXCR2 (-10.1 kcal/mol). MD simulations confirmed stable binding of the CXCR2-Navarixin complex. qRT-PCR confirmed significant downregulation of all three genes in IPAH patients.

  Conclusion: This hypothesis-generating study identifies shared transcriptomic signatures between IPAH and MPM, highlighting CXCR2, S100A9, and LCN2 as candidate biomarkers linked to immune dysregulation and metabolic reprogramming. The computational and correlative nature of these findings, together with the limited size of the external validation cohort, requires confirmation through functional experiments and validation in larger, independent, and multicentre cohorts before clinical translation can be considered.

  Copyright © 2026 Zhang, Wang, Wang, Guo, Yu, Wang, Luo and Wu.

• A comprehensive pancancer analysis reveals the potential value of RAR-related orphan receptor C (RORC) for cancer immunotherapy. S. He, J. Yu, W. Sun, et al. 2022;13:969476. PubMed · Publisher · Free full text

  Abstract

  Background: RAR-related orphan receptor C (RORC) plays an important role in autoimmune responses and inflammation. However, its function in cancer immunity is still unclear. Its potential value in cancer immunotherapy (CIT) needs to be further studied. Methods: Expression and clinical data for 33 cancers were obtained from UCSC-Xena. The correlation between RORC expression and clinical parameters was analyzed using the limma software package to assess the prognostic value of RORC. Timer2.0 and DriverDBv3 were used to analyze the RORC mutation and methylation profiles. RORC-associated signaling pathways were identified by GSEA. The correlations of RORC expression with tumor microenvironment factors were further assessed, including immune cell infiltration (obtained by CIBERSORT) and immunomodulators (in pancancer datasets from the Tumor-Immune System Interactions and Drug Bank [TISIDB] database). In addition, the correlations of RORC with four CIT biomarkers (tumor mutational burden, microsatellite instability, programmed death ligand-1, and mismatch repair) were explored. Furthermore, three CIT cohorts (GSE67501, GSE168204, and IMvigor210) from the Gene Expression Omnibus database and a previously published study were used to determine the association between RORC expression and CIT response. Results: RORC was differentially expressed in many tumor tissues relative to normal tissues (20/33). In a small number of cancers, RORC expression was correlated with age (7/33), sex (4/33), and tumor stage (9/33). Furthermore, RORC expression showed prognostic value in many cancers, especially in kidney renal clear cell carcinoma (KIRC), brain lower grade glioma (LGG), and mesothelioma (MESO). The mutation rate of RORC in most cancer types was low, while RORC was hypermethylated or hypomethylated in multiple cancers. RORC was associated with a variety of biological processes and signal transduction pathways in various cancers. Furthermore, RORC was strongly correlated with immune cell infiltration, immunomodulators, and CIT biomarkers. However, no significant association was found between RORC and CIT response in the three CIT cohorts. Conclusion Our findings revealed the potential immunotherapeutic value of RORC for various cancers and provides preliminary evidence for the application of RORC in CIT.

  Copyright © 2022 He, Yu, Sun, Sun, Tang, Meng, Liu and Li.

• NFE2L3 as a Novel Biomarker Associated With IL-2/STAT5/NLRP3 Signaling Pathway in Malignant Pleural Mesothelioma and Other Cancers. Z. Wang, H. Yang, B. Luo, et al. 2022;13:805256. PubMed · Publisher · Free full text

  Abstract

  Background: Malignant pleural mesothelioma (MPM) is a malignant tumor originating from pleural mesothelial cells and has a high mortality rate worldwide. With the advent of immunotherapy in MPM treatment, there is an urgent need to elucidate the immune-related mechanisms in this caner. Methods: Single-sample gene set enrichment analysis (ssGSEA) was used to score the immunocytes infiltration of data from different database sources. Identification of immunocyte-related genes was performed with weighted gene co-expression network analysis (WGCNA), differentially expressed genes (DEGs) analysis, and correlation analysis. Pan-caner analysis was performed using "DiffExp" and "Correlation" modules in TIMER. Results: T-helper 2 (Th2) cell was found to be a poor prognostic factor for patients with MPM. Then a transcription factor, NFE2L3, was identified as a biomarker that showed a strong positive correlation with Th2 cell infiltration, and was highly expressed in MPM tissues and was related to the poor prognosis of these patients. At the same time, multiple NFE2L3 methylation sites were negatively correlated with Th2 cell infiltration, and patients with a high degree of methylation enjoy a better prognosis. Pan-caner analysis indicated that NFE2L3 might promote the differentiation of Th2 cells through the IL-2/STAT5/NLRP3 signaling pathway in MPM and many other cancers. Conclusion: We believe that NFE2L3 can serve as a potential biomarker related to the diagnosis and prognosis of patients with MPM, and speculate that NFE2L3 could promote Th2 cell differentiation via IL-2/STAT5/NLRP3 signaling pathway in MPM and many other cancers.

  Copyright © 2022 Wang, Yang, Luo, Duan and Lin.

• Prognostic Value of Germline Copy Number Variants and Environmental Exposures in Non-small Cell Lung Cancer. S. Chen, L. Lu, J. Xian, et al. 2021;12:681857. PubMed · Publisher · Free full text

  Abstract

  Germline copy number variant (gCNV) has been studied as a genetic determinant for prognosis of several types of cancer, but little is known about how it affects non-small cell lung cancer (NSCLC) prognosis. We aimed to develop a prognostic nomogram for NSCLC based on gCNVs. Promising gCNVs that are associated with overall survival (OS) of NSCLC were sorted by analyzing the TCGA data and were validated in a small Chinese population. Then the successfully verified gCNVs were determined in a training cohort (n = 570) to develop a prognostic nomogram, and in a validation cohort (n = 465) to validate the nomogram. Thirty-five OS-related gCNVs were sorted and were reduced to 15 predictors by the Lasso regression analysis. Of them, only CNVR395.1 and CNVR2239.1 were confirmed to be associated with OS of NSCLC in the Chinese population. High polygenic risk score (PRS), which was calculated by the hazard effects of CNVR395.1 and CNVR2239.1, exerted a significantly higher death rate in the training cohort (HR = 1.41, 95%CI: 1.16-1.74) and validation cohort (HR = 1.42, 95%CI: 1.13-1.77) than low PRS. The nomogram incorporating PRS and surrounding factors, achieved admissible concordance indexes of 0.678 (95%CI: 0.664-0.693) and 0.686 (95%CI: 0.670-0.702) in predicting OS in the training and validation cohorts, respectively, and had well-fitted calibration curves. Moreover, an interaction between PRS and asbestos exposure was observed on affecting OS (P interaction = 0.042). Our analysis developed a nomogram that achieved an admissible prediction of NSCLC survival, which would be beneficial to the personalized intervention of NSCLC.

  Copyright © 2021 Chen, Lu, Xian, Shi, Chen, Rao, Qiu, Lu and Yang.

• Identification of a Five-Gene Signature for Predicting Survival in Malignant Pleural Mesothelioma Patients. Y. Bai, X. Wang, J. Hou, et al. 2020;11:899. PubMed · Publisher · Free full text

  Abstract

  Malignant pleural mesothelioma (MPM), predominantly caused by asbestos exposure, is a highly aggressive cancer with poor prognosis. The staging systems currently used in clinics is inadequate in evaluating the prognosis of MPM. In this study, a five-gene signature was developed and enrolled into a prognostic risk score model by LASSO Cox regression analysis based on two expression profiling datasets (GSE2549 and GSE51024) from Gene Expression Omnibus (GEO). The five-gene signature was further validated using the Cancer Genome Atlas (TCGA) MPM dataset. Univariate and multivariate Cox analyses proved that the five-gene signature was an independent prognostic factor for MPM. The signature remained statistically significant upon stratification by Brigham stage, AJCC stage, gender, tumor size, and lymph node status. Time-dependent receiver operating characteristic (ROC) curve indicated good performance of our model in predicting 1- and 2-years overall survival in MPM patients. The C-index was 0.784 for GSE2549 and 0.753 for the TCGA dataset showing moderate predictive accuracy of our model. Furthermore, Gene Set Enrichment Analysis suggested that the five-gene signature was related to pathways resulting in MPM tumor progression. Together, we have established a five-gene signature significantly associated with prognosis in MPM patients. Hence, the five-genes signature may serve as a potentially useful prognostic tool for MPM patients.

  Copyright © 2020 Bai, Wang, Hou, Geng, Liang, Ruan, Guo, Nan and Jiang.

• Variation rs2235503 C > A Within the Promoter of MSLN Affects Transcriptional Rate of Mesothelin and Plasmatic Levels of the Soluble Mesothelin-Related Peptide. R. Silvestri, P. Pucci, C. De Santi, et al. 2020;11:975. PubMed · Publisher · Free full text

  Abstract

  Soluble mesothelin-related peptide (SMRP) is a promising biomarker for malignant pleural mesothelioma (MPM), but several confounding factors can reduce SMRP-based test's accuracy. The identification of these confounders could improve the diagnostic performance of SMRP. In this study, we evaluated the sequence of 1,000 base pairs encompassing the minimal promoter region of the MSLN gene to identify expression quantitative trait loci (eQTL) that can affect SMRP. We assessed the association between four MSLN promoter variants and SMRP levels in a cohort of 72 MPM and 677 non-MPM subjects, and we carried out in vitro assays to investigate their functional role. Our results show that rs2235503 is an eQTL for MSLN associated with increased levels of SMRP in non-MPM subjects. Furthermore, we show that this polymorphic site affects the accuracy of SMRP, highlighting the importance of evaluating the individual's genetic background and giving novel insights to refine SMRP specificity as a diagnostic biomarker.

  Copyright © 2020 Silvestri, Pucci, De Santi, Dell’Anno, Miglietta, Corrado, Nicolí, Marolda, Cipollini, Pellegrino, Evangelista, Bonotti, Foddis, Cristaudo, Landi and Gemignani.

2010s

• Hedgehog Signaling in Mesothelioma: 2019 Status. E. Felley-Bosco. 2019;10:1121. PubMed · Publisher · Free full text

• Macrophage Depletion in Elderly Mice Improves Response to Tumor Immunotherapy, Increases Anti-tumor T Cell Activity and Reduces Treatment-Induced Cachexia. L. Duong, H.G. Radley-Crabb, J.K. Gardner, et al. 2018;9:526. PubMed · Publisher · Free full text

  Abstract

  Most cancers emerge in the elderly, including lung cancer and mesothelioma, yet the elderly remain an underrepresented population in pre-clinical cancer studies and clinical trials. The immune system plays a critical role in the effectiveness of many anti-cancer therapies in young hosts via tumor-specific T cells. However, immunosuppressive macrophages can constitute up to 50% of the tumor burden and impair anti-tumor T cell activity. Altered macrophage phenotype and function during aging may further impact anti-tumor T cell responses. Yet, the impact of macrophages on anti-tumor T cell responses and immunotherapy in the elderly is unknown. Therefore, we examined macrophages and their interaction with T cells in young (3 months) and elderly (20-24 months) AE17 mesothelioma-bearing female C57BL/6J mice during tumor growth. Mesothelioma tumors grew faster in elderly compared with young mice, and this corresponded with an increase in tumor-associated macrophages. During healthy aging, macrophages increase in bone marrow and spleens suggesting that these sites have an increased potential to supply cancer-promoting macrophages. Interestingly, in tumor-bearing mice, bone marrow macrophages increased proliferation whilst splenic macrophages had reduced proliferation in elderly compared with young mice, and macrophage depletion using the F4/80 antibody slowed tumor growth in young and elderly mice. We also examined responses to treatment with intra-tumoral IL-2/anti-CD40 antibody immunotherapy and found it was less effective in elderly (38% tumor regression) compared to young mice (90% regression). Tumor-bearing elderly mice decreased in vivo anti-tumor cytotoxic T cell activity in tumor draining lymph nodes and spleens. Depletion of macrophages using F4/80 antibody in elderly, but not young mice, improved IL-2/anti-CD40 immunotherapy up to 78% tumor regression. Macrophage depletion also increased in vivo anti-tumor T cell activity in elderly, but not young mice. All the tumor-bearing elderly (but not young) mice had decreased body weight (i.e., exhibited cachexia), which was greatly exacerbated by immunotherapy; whereas macrophage depletion prevented this immunotherapy-induced cachexia. These studies strongly indicate that age-related changes in macrophages play a key role in driving cancer cachexia in the elderly, particularly during immunotherapy, and sabotage elderly anti-tumor immune responses.

• Pre-clinical Models for Malignant Mesothelioma Research: From Chemical-Induced to Patient-Derived Cancer Xenografts. N. Nabavi, J. Wei, D. Lin, et al. 2018;9:232. Review PubMed · Publisher · Free full text

  Abstract

  Malignant mesothelioma (MM) is a rare disease often associated with environmental exposure to asbestos and other erionite fibers. MM has a long latency period prior to manifestation and a poor prognosis. The survival post-diagnosis is often less than a year. Although use of asbestos has been banned in the United States and many European countries, asbestos is still being used and extracted in many developing countries. Occupational exposure to asbestos, mining, and migration are reasons that we expect to continue to see growing incidence of mesothelioma in the coming decades. Despite improvements in survival achieved with multimodal therapies and cytoreductive surgeries, less morbid, more effective interventions are needed. Thus, identifying prognostic and predictive biomarkers for MM, and developing novel agents for targeted therapy, are key unmet needs in mesothelioma research and treatment. In this review, we discuss the evolution of pre-clinical model systems developed to study MM and emphasize the remarkable capability of patient-derived xenograft (PDX) MM models in expediting the pre-clinical development of novel therapeutic approaches. PDX disease model systems retain major characteristics of original malignancies with high fidelity, including molecular, histopathological and functional heterogeneities, and as such play major roles in translational research, drug development, and precision medicine.

• Posttranscriptional Regulation Controls Calretinin Expression in Malignant Pleural Mesothelioma. J. Kresoja-Rakic, M. Sulemani, M.B. Kirschner, et al. 2017;8:70. PubMed · Publisher · Free full text

  Abstract

  Calretinin (CALB2) is a diagnostic and prognostic marker in malignant pleural mesothelioma (MPM). We previously reported that calretinin expression is regulated at the mRNA level. The presence of a medium-sized (573 nucleotide) 3' untranslated region (3'UTR) predicted to contain binding sites for miR-30a/b/c/d/e and miR-9 as well as an adenine/uridine-rich element (ARE) in all three transcripts arising from the CALB2 gene, suggests that calretinin expression is regulated via posttranscriptional mechanisms. Our aim was to investigate the role of the CALB2-3'UTR in the posttranscriptional regulation of calretinin expression in MPM. CALB2-3'UTR was inserted downstream of the luciferase reporter gene using pmiRGLO vector and reporter expression was determined after transfection into MPM cells. Targeted mutagenesis was used to generate variants harboring mutated miR-30 family and ARE binding sites. Electrophoretic mobility shift assay was used to test for the presence of ARE binding proteins. CALB2-3'UTR significantly decreased luciferase activity in MPM cells. Analysis of mutation in the ARE site revealed a further destabilization of the reporter and human antigen R (HuR) binding to the ARE sequence was detected. The mutation of two miR-30 binding sites abolished CALB2-3'UTR destabilization effect; a transient delivery of miR-30e-5p mimics or anti-miR into MPM cells resulted in a significant decrease/increase of the luciferase reporter expression and calretinin protein, respectively. Moreover, overexpression of CALB2-3'UTR quenched the effect of miR-30e-5p mimics on calretinin protein levels, possibly by sequestering the mimics, thereby suggesting a competitive endogenous RNA network. Finally, by data mining we observed that expression of miR-30e-5p was negatively correlated with the calretinin expression in a cohort of MPM patient samples. Our data show the role of (1) adenine-uridine (AU)-binding proteins in calretinin stabilization and (2) miR-30e-5p in the posttranscriptional negative regulation of calretinin expression via interaction with its 3'UTR. Furthermore, our study demonstrates a possible physiological role of calretinin's alternatively spliced transcripts.

• Tumors that mimic asbestos-related mesothelioma: time to consider a genetics-based tumor registry?. B.D. Kerger, R.C. James, D.A. Galbraith. 2014;5:151. PubMed · Publisher · Free full text

  Abstract

  The diagnosis of mesothelioma is not always straightforward, despite known immunohistochemical markers and other diagnostic techniques. One reason for the difficulty is that extrapleural tumors resembling mesothelioma may have several possible etiologies, especially in cases with no meaningful history of amphibole asbestos exposure. When the diagnosis of mesothelioma is based on histologic features alone, primary mesotheliomas may resemble various primary or metastatic cancers that have directly invaded the serosal membranes. Some of these metastatic malignancies, particularly carcinomas and sarcomas of the pleura, pericardium and peritoneum, may undergo desmoplastic reaction in the pleura, thereby mimicking mesothelioma, rather than the primary tumor. Encasement of the lung by direct spread or metastasis, termed pseudomesotheliomatous spread, occurs with several other primary cancer types, including certain late-stage tumors from genetic cancer syndromes exhibiting chromosomal instability. Although immunohistochemical staining patterns differentiate most carcinomas, lymphomas, and mestastatic sarcomas from mesotheliomas, specific genetic markers in tumor or somatic tissues have been recently identified that may also distinguish these tumor types from asbestos-related mesothelioma. A registry for genetic screening of mesothelioma cases would help lead to improvements in diagnostic criteria, prognostic accuracy and treatment efficacy, as well as improved estimates of primary mesothelioma incidence and of background rates of cancers unrelated to asbestos that might be otherwise mistaken for mesothelioma. This information would also help better define the dose-response relationships for mesothelioma and asbestos exposure, as well as other risk factors for mesothelioma and other mesenchymal or advanced metastatic tumors that may be indistinguishable by histology and staining characteristics.

• Epigenomics in environmental health. B.C. Christensen, C.J. Marsit. 2011;2:84. PubMed · Publisher · Free full text

  Abstract

  This review considers the emerging relationships between environmental factors and epigenetic alterations and the application of genome-wide assessments to better define these relationships. First we will briefly cover epigenetic programming in development, one-carbon metabolism, and exposures that may disrupt normal developmental programming of epigenetic states. In addition, because a large portion of epigenetic research has focused on cancer, we discuss exposures associated with carcinogenesis including asbestos, alcohol, radiation, arsenic, and air pollution. Research on other exposures that may affect epigenetic states such as endocrine disruptors is also described, and we also review the evidence for epigenetic alterations associated with aging that may reflect cumulative effects of exposures. From this evidence, we posit potential mechanisms by which exposures modify epigenetic states, noting that understanding the true effect of environmental exposures on the human epigenome will require additional research with appropriate epidemiologic studies and application of novel technologies. With a more comprehensive understanding of the affects of exposures on the epigenome, including consideration of genetic background, the prediction of the toxic potential of new compounds may be more readily achieved, and may lead to the development of more personalized disease prevention and treatment strategies.

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