Aop: 409


Each AOP should be given a descriptive title that takes the form “MIE leading to AO”. For example, “Aromatase inhibition [MIE] leading to reproductive dysfunction [AO]” or “Thyroperoxidase inhibition [MIE] leading to decreased cognitive function [AO]”. In cases where the MIE is unknown or undefined, the earliest known KE in the chain (i.e., furthest upstream) should be used in lieu of the MIE and it should be made clear that the stated event is a KE and not the MIE. More help

Frustrated phagocytosis leads to malignant mesothelioma

Short name
A short name should also be provided that succinctly summarises the information from the title. This name should not exceed 90 characters. More help
Frustrated phagocytosis leads to malignant mesothelioma

Graphical Representation

A graphical summary of the AOP listing all the KEs in sequence, including the MIE (if known) and AO, and the pair-wise relationships (links or KERs) between those KEs should be provided. This is easily achieved using the standard box and arrow AOP diagram (see this page for example). The graphical summary is prepared and uploaded by the user (templates are available) and is often included as part of the proposal when AOP development projects are submitted to the OECD AOP Development Workplan. The graphical representation or AOP diagram provides a useful and concise overview of the KEs that are included in the AOP, and the sequence in which they are linked together. This can aid both the process of development, as well as review and use of the AOP (for more information please see page 19 of the Users' Handbook).If you already have a graphical representation of your AOP in electronic format, simple save it in a standard image format (e.g. jpeg, png) then click ‘Choose File’ under the “Graphical Representation” heading, which is part of the Summary of the AOP section, to select the file that you have just edited. Files must be in jpeg, jpg, gif, png, or bmp format. Click ‘Upload’ to upload the file. You should see the AOP page with the image displayed under the “Graphical Representation” heading. To remove a graphical representation file, click 'Remove' and then click 'OK.'  Your graphic should no longer be displayed on the AOP page. If you do not have a graphical representation of your AOP in electronic format, a template is available to assist you.  Under “Summary of the AOP”, under the “Graphical Representation” heading click on the link “Click to download template for graphical representation.” A Powerpoint template file should download via the default download mechanism for your browser. Click to open this file; it contains a Powerpoint template for an AOP diagram and instructions for editing and saving the diagram. Be sure to save the diagram as jpeg, jpg, gif, png, or bmp format. Once the diagram is edited to its final state, upload the image file as described above. More help


List the name and affiliation information of the individual(s)/organisation(s) that created/developed the AOP. In the context of the OECD AOP Development Workplan, this would typically be the individuals and organisation that submitted an AOP development proposal to the EAGMST. Significant contributors to the AOP should also be listed. A corresponding author with contact information may be provided here. This author does not need an account on the AOP-KB and can be distinct from the point of contact below. The list of authors will be included in any snapshot made from an AOP. More help

Nureddin K. Mansour, Università degli Studi, Milan, Italy

Merlin Mei, Environmental Protection Agency, US

Marvin Martens, Maastricht University, Netherlands

Franziska Kreidl, Maastricht University, Netherlands

Holly Mortensen, Environmental Protection Agency, US

Penny Nymark, Insititute of Environmental Medicine, Karolinska Insitutet, Sweden

Point of Contact

Indicate the point of contact for the AOP-KB entry itself. This person is responsible for managing the AOP entry in the AOP-KB and controls write access to the page by defining the contributors as described below. Clicking on the name will allow any wiki user to correspond with the point of contact via the email address associated with their user profile in the AOP-KB. This person can be the same as the corresponding author listed in the authors section but isn’t required to be. In cases where the individuals are different, the corresponding author would be the appropriate person to contact for scientific issues whereas the point of contact would be the appropriate person to contact about technical issues with the AOP-KB entry itself. Corresponding authors and the point of contact are encouraged to monitor comments on their AOPs and develop or coordinate responses as appropriate.  More help
Evgeniia Kazymova   (email point of contact)


List user names of all  authors contributing to or revising pages in the AOP-KB that are linked to the AOP description. This information is mainly used to control write access to the AOP page and is controlled by the Point of Contact.  More help
  • Nureddin Mansour
  • Penny Nymark
  • Merlin Mei
  • Evgeniia Kazymova


The status section is used to provide AOP-KB users with information concerning how actively the AOP page is being developed, what type of use or input the authors feel comfortable with given the current level of development, and whether it is part of the OECD AOP Development Workplan and has been reviewed and/or endorsed. “Author Status” is an author defined field that is designated by selecting one of several options from a drop-down menu (Table 3). The “Author Status” field should be changed by the point of contact, as appropriate, as AOP development proceeds. See page 22 of the User Handbook for definitions of selection options. More help
Author status OECD status OECD project SAAOP status
Under development: Not open for comment. Do not cite
This AOP was last modified on May 08, 2022 11:33
The date the AOP was last modified is automatically tracked by the AOP-KB. The date modified field can be used to evaluate how actively the page is under development and how recently the version within the AOP-Wiki has been updated compared to any snapshots that were generated. More help

Revision dates for related pages

Page Revision Date/Time
Frustrated phagoytosis August 13, 2019 04:48
Increased, secretion of proinflammatory mediators January 25, 2022 15:50
Increased, recruitment of inflammatory cells January 25, 2022 15:52
Increased, Reactive oxygen species November 27, 2017 13:15
Increased, DNA damage and mutation August 13, 2019 05:41
Genomic instability July 06, 2021 06:05
Increase, Cell Proliferation June 23, 2021 12:28
Increased, mesotheliomas December 03, 2016 16:37
Frustrated phagoytosis leads to Increased proinflammatory mediators July 06, 2021 06:10
Frustrated phagoytosis leads to Increased, Reactive oxygen species July 06, 2021 06:11
Increased proinflammatory mediators leads to Recruitment of inflammatory cells December 07, 2021 10:28
Recruitment of inflammatory cells leads to Increased, Reactive oxygen species July 03, 2019 11:53
Increased, Reactive oxygen species leads to Increased, DNA damage and mutation July 03, 2019 11:53
Increased, DNA damage and mutation leads to Genomic instability July 06, 2021 06:12
Genomic instability leads to Increase, Cell Proliferation July 06, 2021 06:12
Increase, Cell Proliferation leads to Increased, mesotheliomas July 06, 2021 06:13
Multi-walled carbon nanotubes July 26, 2017 18:59
Asbestos fibers September 02, 2021 09:31


In the abstract section, authors should provide a concise and informative summation of the AOP under development that can stand-alone from the AOP page. Abstracts should typically be 200-400 words in length (similar to an abstract for a journal article). Suggested content for the abstract includes the following: The background/purpose for initiation of the AOP’s development (if there was a specific intent) A brief description of the MIE, AO, and/or major KEs that define the pathway A short summation of the overall WoE supporting the AOP and identification of major knowledge gaps (if any) If a brief statement about how the AOP may be applied (optional). The aim is to capture the highlights of the AOP and its potential scientific and regulatory relevance More help

This AOP starts with frustrated phagocytosis, meaning that macrophages fail to engulf long fibers and die with a concomitant massive release of ROS and pro-inflammatory signals. Any fibre that exceeds a maximum length for macrophage uptake will result in frustrated phagocytosis. The release of ROS and pro-inflammatory signals together with persistent cytotoxicity and tissue injury in the pleura can lead to secondary genotoxicity, including oxidative lesions to DNA. When DNA repair pathways are overwhelmed and the DNA lesions exceed the repair capacity, it may lead to mutagenesis with increased mutations and DNA double strand breaks. Increased DNA damage increases the risk for genomic instability and accumulation of mutations in mesothelial cells. Specific mutations and chromosomal aberrations have been associated with mesothelioma, including for example mutation of BAP1 and other genes, and  loss of chromosomal regions 3p21 (which harbours the BAP1 gene) and 9p21. These mutations and deletions are assumed to be involved in the molecular and genetic alterations that drive mesothelial cell proliferation, which is the final key event leading to the adverse outcome: malignant pleural mesothelioma.

There is abundant evidence for this process taking place in humans exposed to asbestos fibres. Recently, experimental evidence from both in vivo and in vitro studies indicate that a similar process may take place in humans exposed to cetrain types of nanomaterials with high aspect ratios, such as multi-walled carbon nanotubes.

Background (optional)

This optional subsection should be used to provide background information for AOP reviewers and users that is considered helpful in understanding the biology underlying the AOP and the motivation for its development. The background should NOT provide an overview of the AOP, its KEs or KERs, which are captured in more detail below. Examples of potential uses of the optional background section are listed on pages 24-25 of the User Handbook. More help

Summary of the AOP

This section is for information that describes the overall AOP. The information described in section 1 is entered on the upper portion of an AOP page within the AOP-Wiki. This is where some background information may be provided, the structure of the AOP is described, and the KEs and KERs are listed. More help


Molecular Initiating Events (MIE)
An MIE is a specialised KE that represents the beginning (point of interaction between a stressor and the biological system) of an AOP. More help
Key Events (KE)
This table summarises all of the KEs of the AOP. This table is populated in the AOP-Wiki as KEs are added to the AOP. Each table entry acts as a link to the individual KE description page.  More help
Adverse Outcomes (AO)
An AO is a specialised KE that represents the end (an adverse outcome of regulatory significance) of an AOP.  More help
Sequence Type Event ID Title Short name
MIE 1668 Frustrated phagoytosis Frustrated phagoytosis
KE 1497 Increased, recruitment of inflammatory cells Recruitment of inflammatory cells
KE 1496 Increased, secretion of proinflammatory mediators Increased proinflammatory mediators
KE 1115 Increased, Reactive oxygen species Increased, Reactive oxygen species
KE 1669 Increased, DNA damage and mutation Increased, DNA damage and mutation
KE 1896 Genomic instability Genomic instability
KE 870 Increase, Cell Proliferation Increase, Cell Proliferation
AO 1090 Increased, mesotheliomas Increased, mesotheliomas

Relationships Between Two Key Events (Including MIEs and AOs)

This table summarises all of the KERs of the AOP and is populated in the AOP-Wiki as KERs are added to the AOP. Each table entry acts as a link to the individual KER description page.To add a key event relationship click on either Add relationship: events adjacent in sequence or Add relationship: events non-adjacent in sequence.For example, if the intended sequence of KEs for the AOP is [KE1 > KE2 > KE3 > KE4]; relationships between KE1 and KE2; KE2 and KE3; and KE3 and KE4 would be defined using the add relationship: events adjacent in sequence button.  Relationships between KE1 and KE3; KE2 and KE4; or KE1 and KE4, for example, should be created using the add relationship: events non-adjacent button. This helps to both organize the table with regard to which KERs define the main sequence of KEs and those that provide additional supporting evidence and aids computational analysis of AOP networks, where non-adjacent KERs can result in artifacts (see Villeneuve et al. 2018; DOI: 10.1002/etc.4124).After clicking either option, the user will be brought to a new page entitled ‘Add Relationship to AOP.’ To create a new relationship, select an upstream event and a downstream event from the drop down menus. The KER will automatically be designated as either adjacent or non-adjacent depending on the button selected. The fields “Evidence” and “Quantitative understanding” can be selected from the drop-down options at the time of creation of the relationship, or can be added later. See the Users Handbook, page 52 (Assess Evidence Supporting All KERs for guiding questions, etc.).  Click ‘Create [adjacent/non-adjacent] relationship.’  The new relationship should be listed on the AOP page under the heading “Relationships Between Two Key Events (Including MIEs and AOs)”. To edit a key event relationship, click ‘Edit’ next to the name of the relationship you wish to edit. The user will be directed to an Editing Relationship page where they can edit the Evidence, and Quantitative Understanding fields using the drop down menus. Once finished editing, click ‘Update [adjacent/non-adjacent] relationship’ to update these fields and return to the AOP page.To remove a key event relationship to an AOP page, under Summary of the AOP, next to “Relationships Between Two Key Events (Including MIEs and AOs)” click ‘Remove’ The relationship should no longer be listed on the AOP page under the heading “Relationships Between Two Key Events (Including MIEs and AOs)”. More help

Network View

The AOP-Wiki automatically generates a network view of the AOP. This network graphic is based on the information provided in the MIE, KEs, AO, KERs and WoE summary tables. The width of the edges representing the KERs is determined by its WoE confidence level, with thicker lines representing higher degrees of confidence. This network view also shows which KEs are shared with other AOPs. More help


The stressor field is a structured data field that can be used to annotate an AOP with standardised terms identifying stressors known to trigger the MIE/AOP. Most often these are chemical names selected from established chemical ontologies. However, depending on the information available, this could also refer to chemical categories (i.e., groups of chemicals with defined structural features known to trigger the MIE). It can also include non-chemical stressors such as genetic or environmental factors. Although AOPs themselves are not chemical or stressor-specific, linking to stressor terms known to be relevant to different AOPs can aid users in searching for AOPs that may be relevant to a given stressor. More help

Life Stage Applicability

Identify the life stage for which the KE is known to be applicable. More help

Taxonomic Applicability

Latin or common names of a species or broader taxonomic grouping (e.g., class, order, family) can be selected. In many cases, individual species identified in these structured fields will be those for which the strongest evidence used in constructing the AOP was available in relation to this KE. More help

Sex Applicability

The authors must select from one of the following: Male, female, mixed, asexual, third gender, hermaphrodite, or unspecific. More help

Overall Assessment of the AOP

This section addresses the relevant biological domain of applicability (i.e., in terms of taxa, sex, life stage, etc.) and WoE for the overall AOP as a basis to consider appropriate regulatory application (e.g., priority setting, testing strategies or risk assessment). The goal of the overall assessment is to provide a high level synthesis and overview of the relative confidence in the AOP and where the significant gaps or weaknesses are (if they exist). Users or readers can drill down into the finer details captured in the KE and KER descriptions, and/or associated summary tables, as appropriate to their needs.Assessment of the AOP is organised into a number of steps. Guidance on pages 59-62 of the User Handbook is available to facilitate assignment of categories of high, moderate, or low confidence for each consideration. While it is not necessary to repeat lengthy text that appears elsewhere in the AOP description (or related KE and KER descriptions), a brief explanation or rationale for the selection of high, moderate, or low confidence should be made. More help

Domain of Applicability

The relevant biological domain(s) of applicability in terms of sex, life-stage, taxa, and other aspects of biological context are defined in this section. Biological domain of applicability is informed by the “Description” and “Biological Domain of Applicability” sections of each KE and KER description (see sections 2G and 3E for details). In essence the taxa/life-stage/sex applicability is defined based on the groups of organisms for which the measurements represented by the KEs can feasibly be measured and the functional and regulatory relationships represented by the KERs are operative.The relevant biological domain of applicability of the AOP as a whole will nearly always be defined based on the most narrowly restricted of its KEs and KERs. For example, if most of the KEs apply to either sex, but one is relevant to females only, the biological domain of applicability of the AOP as a whole would be limited to females. While much of the detail defining the domain of applicability may be found in the individual KE and KER descriptions, the rationale for defining the relevant biological domain of applicability of the overall AOP should be briefly summarised on the AOP page. More help

Essentiality of the Key Events

An important aspect of assessing an AOP is evaluating the essentiality of its KEs. The essentiality of KEs can only be assessed relative to the impact of manipulation of a given KE (e.g., experimentally blocking or exacerbating the event) on the downstream sequence of KEs defined for the AOP. Consequently evidence supporting essentiality is assembled on the AOP page, rather than on the independent KE pages that are meant to stand-alone as modular units without reference to other KEs in the sequence.The nature of experimental evidence that is relevant to assessing essentiality relates to the impact on downstream KEs and the AO if upstream KEs are prevented or modified. This includes: Direct evidence: directly measured experimental support that blocking or preventing a KE prevents or impacts downstream KEs in the pathway in the expected fashion. Indirect evidence: evidence that modulation or attenuation in the magnitude of impact on a specific KE (increased effect or decreased effect) is associated with corresponding changes (increases or decreases) in the magnitude or frequency of one or more downstream KEs.When assembling the support for essentiality of the KEs, authors should organise relevant data in a tabular format. The objective is to summarise briefly the nature and numbers of investigations in which the essentiality of KEs has been experimentally explored either directly or indirectly. See pages 50-51 in the User Handbook for further definitions and clarifications.  More help

Evidence Assessment

The biological plausibility, empirical support, and quantitative understanding from each KER in an AOP are assessed together.  Biological plausibility of each of the KERs in the AOP is the most influential consideration in assessing WoE or degree of confidence in an overall hypothesised AOP for potential regulatory application (Meek et al., 2014; 2014a). Empirical support entails consideration of experimental data in terms of the associations between KEs – namely dose-response concordance and temporal relationships between and across multiple KEs. It is examined most often in studies of dose-response/incidence and temporal relationships for stressors that impact the pathway. While less influential than biological plausibility of the KERs and essentiality of the KEs, empirical support can increase confidence in the relationships included in an AOP. For clarification on how to rate the given empirical support for a KER, as well as examples, see pages 53- 55 of the User Handbook.  More help

Quantitative Understanding

Some proof of concept examples to address the WoE considerations for AOPs quantitatively have recently been developed, based on the rank ordering of the relevant Bradford Hill considerations (i.e., biological plausibility, essentiality and empirical support) (Becker et al., 2017; Becker et al, 2015; Collier et al., 2016). Suggested quantitation of the various elements is expert derived, without collective consideration currently of appropriate reporting templates or formal expert engagement. Though not essential, developers may wish to assign comparative quantitative values to the extent of the supporting data based on the three critical Bradford Hill considerations for AOPs, as a basis to contribute to collective experience.Specific attention is also given to how precisely and accurately one can potentially predict an impact on KEdownstream based on some measurement of KEupstream. This is captured in the form of quantitative understanding calls for each KER. See pages 55-56 of the User Handbook for a review of quantitative understanding for KER's. More help

Considerations for Potential Applications of the AOP (optional)

At their discretion, the developer may include in this section discussion of the potential applications of an AOP to support regulatory decision-making. This may include, for example, possible utility for test guideline development or refinement, development of integrated testing and assessment approaches, development of (Q)SARs / or chemical profilers to facilitate the grouping of chemicals for subsequent read-across, screening level hazard assessments or even risk assessment. While it is challenging to foresee all potential regulatory application of AOPs and any application will ultimately lie within the purview of regulatory agencies, potential applications may be apparent as the AOP is being developed, particularly if it was initiated with a particular application in mind. This optional section is intended to provide the developer with an opportunity to suggest potential regulatory applications and describe his or her rationale.To edit the “Considerations for Potential Applications of the AOP” section, on an AOP page, in the upper right hand menu, click ‘Edit.’ This brings you to a page entitled, “Editing AOP.” Scroll down to the “Considerations for Potential Applications of the AOP” section, where a text entry box allows you to submit text. In the upper right hand menu, click ‘Update AOP’ to save your changes and return to the AOP page or 'Update and continue' to continue editing AOP text sections.  The new text should appear under the “Considerations for Potential Applications of the AOP” section on the AOP page. More help


List the bibliographic references to original papers, books or other documents used to support the AOP. More help
  1. Affar, El Bachir, and Michele Carbone. ‘BAP1 Regulates Different Mechanisms of Cell Death’. Cell Death & Disease 9, no. 12 (December 2018): 1151.
  2. Betti, Marta, Elisabetta Casalone, Daniela Ferrante, Anna Aspesi, Giulia Morleo, Alessandra Biasi, Marika Sculco, et al. ‘Germline Mutations in DNA Repair Genes Predispose Asbestos-Exposed Patients to Malignant Pleural Mesothelioma’. Cancer Letters 405 (1 October 2017): 38–45.
  3. Bott, Matthew, Marie Brevet, Barry S Taylor, Shigeki Shimizu, Tatsuo Ito, Lu Wang, Jenette Creaney, et al. ‘The Nuclear Deubiquitinase BAP1 Is Commonly Inactivated by Somatic Mutations and 3p21.1 Losses in Malignant Pleural Mesothelioma’. Nature Genetics 43, no. 7 (July 2011): 668–72.
  4. Boyles, Matthew S. P., Lesley Young, David M. Brown, Laura MacCalman, Hilary Cowie, Anna Moisala, Fiona Smail, et al. ‘Multi-Walled Carbon Nanotube Induced Frustrated Phagocytosis, Cytotoxicity and pro-Inflammatory Conditions in Macrophages Are Length Dependent and Greater than That of Asbestos’. Toxicology in Vitro 29, no. 7 (1 October 2015): 1513–28.
  5. Bryant, P.E. ‘Enzymatic Restriction of Mammalian Cell DNA Using Pvu II and Bam H1: Evidence for the Double-Strand Break Origin of Chromosomal Aberrations’. International Journal of Radiation Biology and Related Studies in Physics, Chemistry and Medicine 46, no. 1 (January 1984): 57–65.
  6. Chernova, Tatyana. ‘Long-Fiber Carbon Nanotubes Replicate Asbestos-Induced Mesothelioma with Disruption of the Tumor Suppressor Gene Cdkn2a (Ink4a/Arf)’, n.d., 20.
  7. Chew, Shan Hwu, and Shinya Toyokuni. ‘Malignant Mesothelioma as an Oxidative Stress-Induced Cancer: An Update’. Free Radical Biology and Medicine 86 (1 September 2015): 166–78.
  8. Donaldson, Ken, Fiona A. Murphy, Rodger Duffin, and Craig A. Poland. ‘Asbestos, Carbon Nanotubes and the Pleural Mesothelium: A Review of the Hypothesis Regarding the Role of Long Fibre Retention in the Parietal Pleura, Inflammation and Mesothelioma’. Particle and Fibre Toxicology 7, no. 1 (22 March 2010): 5.
  9. Emerce, Esra, Manosij Ghosh, Deniz Öner, Radu-Corneliu Duca, Jeroen Vanoirbeek, Bram Bekaert, Peter H. M. Hoet, and Lode Godderis. ‘Carbon Nanotube- and Asbestos-Induced DNA and RNA Methylation Changes in Bronchial Epithelial Cells’. Chemical Research in Toxicology, 23 April 2019, acs.chemrestox.8b00406.
  10. Feldmann, E., V. Schmiemann, W. Goedecke, S. Reichenberger, and P. Pfeiffer. ‘DNA Double-Strand Break Repair in Cell-Free Extracts from Ku80-Deficient Cells: Implications for Ku Serving as an Alignment Factor in Non-Homologous DNA End Joining’. Nucleic Acids Research 28, no. 13 (1 July 2000): 2585–96.
  11. Godleski, John J. ‘Role of Asbestos in Etiology of Malignant Pleural Mesothelioma’. Thoracic Surgery Clinics 14, no. 4 (November 2004): 479–87.
  12. Hylebos, Marieke, Guy Van Camp, Jan P van Meerbeeck, and Ken Op de Beeck. ‘The Genetic Landscape of Malignant Pleural Mesothelioma: Results from Massively Parallel Sequencing’. Journal of Thoracic Oncology 11, no. 10 (1 October 2016): 1615–26.
  13. Kim, Jeong Eun, Deokhoon Kim, Yong Sang Hong, Kyu-pyo Kim, Young Kwang Yoon, Dae Ho Lee, Sang-We Kim, Sung-Min Chun, Se Jin Jang, and Tae Won Kim. ‘Mutational Profiling of Malignant Mesothelioma Revealed Potential Therapeutic Targets in EGFR and NRAS’. Translational Oncology 11, no. 2 (1 April 2018): 268–74.
  14. Kolb, Thorsten, and Aurélie Ernst. ‘Cell-Based Model Systems for Genome Instability: Dissecting the Mechanistic Basis of Chromothripsis in Cancer’. International Journal of Cancer n/a, no. n/a. Accessed 22 June 2021.
  15. Lindberg, Hanna K., Ghita C. -M. Falck, Rajinder Singh, Satu Suhonen, Hilkka Järventaus, Esa Vanhala, Julia Catalán, Peter B. Farmer, Kai M. Savolainen, and Hannu Norppa. ‘Genotoxicity of Short Single-Wall and Multi-Wall Carbon Nanotubes in Human Bronchial Epithelial and Mesothelial Cells in Vitro’. Toxicology, Nanotoxicology, 313, no. 1 (8 November 2013): 24–37.
  16. Malkin, D, F. Li, L. Strong, J. Fraumeni, C. Nelson, D. Kim, J Kassel, et al. ‘Germ Line P53 Mutations in a Familial Syndrome of Breast Cancer, Sarcomas, and Other Neoplasms’. Science 250, no. 4985 (30 November 1990): 1233–38.
  17. Mansfield, Aaron S., Tobias Peikert, James B. Smadbeck, Julia B. M. Udell, Enrique Garcia-Rivera, Laura Elsbernd, Courtney L. Erskine, et al. ‘Neoantigenic Potential of Complex Chromosomal Rearrangements in Mesothelioma’. Journal of Thoracic Oncology 14, no. 2 (1 February 2019): 276–87.
  18. Matsumoto, Shinji, Kazuki Nabeshima, Makoto Hamasaki, Tatsuki Shibuta, and Tsukuru Umemura. ‘Upregulation of MicroRNA-31 Associates with a Poor Prognosis of Malignant Pleural Mesothelioma with Sarcomatoid Component’. Medical Oncology 31, no. 12 (December 2014): 303.
  19. McMahon, Stephen J., Jan Schuemann, Harald Paganetti, and Kevin M. Prise. ‘Mechanistic Modelling of DNA Repair and Cellular Survival Following Radiation-Induced DNA Damage’. Scientific Reports 6, no. 1 (December 2016): 33290.
  20. Møller, Peter, and Nicklas Raun Jacobsen. ‘Weight of Evidence Analysis for Assessing the Genotoxic Potential of Carbon Nanotubes’. Critical Reviews in Toxicology 47, no. 10 (26 November 2017): 871–88.
  21. Morimoto, Yasuo, Hiroto Izumi, and Etsushi Kuroda. ‘Significance of Persistent Inflammation in Respiratory Disorders Induced by Nanoparticles’. Journal of Immunology Research 2014 (2014): 1–8.
  22. Murali, Rajmohan, Thomas Wiesner, and Richard A. Scolyer. ‘Tumours Associated with BAP1 Mutations’. Pathology 45, no. 2 (1 February 2013): 116–26.
  23. Murphy, Fiona A., Anja Schinwald, Craig A. Poland, and Ken Donaldson. ‘The Mechanism of Pleural Inflammation by Long Carbon Nanotubes: Interaction of Long Fibres with Macrophages Stimulates Them to Amplify pro-Inflammatory Responses in Mesothelial Cells’. Particle and Fibre Toxicology 9, no. 1 (3 April 2012): 8.
  24. Nagai, Hirotaka, and Shinya Toyokuni. ‘Biopersistent Fiber-Induced Inflammation and Carcinogenesis: Lessons Learned from Asbestos toward Safety of Fibrous Nanomaterials’. Archives of Biochemistry and Biophysics 502, no. 1 (1 October 2010): 1–7.
  25. Nasu, Masaki, Mitsuru Emi, Sandra Pastorino, Mika Tanji, Amy Powers, Hugh Luk, Francine Baumann, et al. ‘High Incidence of Somatic BAP1 Alterations in Sporadic Malignant Mesothelioma’. Journal of Thoracic Oncology : Official Publication of the International Association for the Study of Lung Cancer 10, no. 4 (April 2015): 565–76.
  26. Natarajan, A.T., F. Darroudi, L.H.F. Mullenders, and M. Meijers. ‘The Nature and Repair of DNA Lesions That Lead to Chromosomal Aberrations Induced by Ionizing Radiations’. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 160, no. 3 (May 1986): 231–36.
  27. Nymark, Penny, Pekka Kohonen, Vesa Hongisto, and Roland C. Grafström. ‘Toxic and Genomic Influences of Inhaled Nanomaterials as a Basis for Predicting Adverse Outcome’. Annals of the American Thoracic Society 15, no. Supplement_2 (April 2018): S91–97.
  28. Nymark, Penny, Harriet Wikman, Tuija Hienonen-Kempas, and Sisko Anttila. ‘Molecular and Genetic Changes in Asbestos-Related Lung Cancer’. Cancer Letters 265, no. 1 (28 June 2008): 1–15.
  29. Oey, Harald, Marissa Daniels, Vandana Relan, Tian Mun Chee, Morgan R Davidson, Ian A Yang, Jonathan J Ellis, Kwun M Fong, Lutz Krause, and Rayleen V Bowman. ‘Whole-Genome Sequencing of Human Malignant Mesothelioma Tumours and Cell Lines’. Carcinogenesis 40, no. 6 (6 July 2019): 724–34.
  30. Pass, Harvey I., Chandra Goparaju, Sergey Ivanov, Jessica Donington, Michele Carbone, Moshe Hoshen, Dalia Cohen, et al. ‘Hsa-Mir-29c* Is Linked to the Prognosis of Malignant Pleural Mesothelioma’. Cancer Research 70, no. 5 (1 March 2010): 1916–24.
  31. Pociask, Derek A, Patricia J Sime, and Arnold R Brody. ‘Asbestos-Derived Reactive Oxygen Species Activate TGF-Β1’. Laboratory Investigation 84, no. 8 (August 2004): 1013–23.
  32. Przybytkowski, Ewa, Elizabeth Lenkiewicz, Michael T Barrett, Kathleen Klein, Sheida Nabavi, Celia MT Greenwood, and Mark Basik. ‘Chromosome-Breakage Genomic Instability and Chromothripsis in Breast Cancer’. BMC Genomics 15, no. 1 (2014): 579.
  33. Schinwald, Anja, and Ken Donaldson. ‘Use of Back-Scatter Electron Signals to Visualise Cell/Nanowires Interactions in Vitro and in Vivo; Frustrated Phagocytosis of Long Fibres in Macrophages and Compartmentalisation in Mesothelial Cells in Vivo’, 2012, 14.
  34. ‘Use of Back-Scatter Electron Signals to Visualise Cell/Nanowires Interactions in Vitro and in Vivo; Frustrated Phagocytosis of Long Fibres in Macrophages and Compartmentalisation in Mesothelial Cells in Vivo’. Particle and Fibre Toxicology 9, no. 1 (28 August 2012): 34.
  35. Siegrist, Katelyn J., Steven H. Reynolds, Dale W. Porter, Robert R. Mercer, Alison K. Bauer, David Lowry, Lorenzo Cena, et al. ‘Mitsui-7, Heat-Treated, and Nitrogen-Doped Multi-Walled Carbon Nanotubes Elicit Genotoxicity in Human Lung Epithelial Cells’. Particle and Fibre Toxicology 16 (7 October 2019).
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