Mechanisms of carcinogenesis and clinical features of asbestos-associated cancers

Our plain-English summary of Mechanisms of carcinogenesis and clinical features of asbestos-associated cancers, by B.T. Mossman, D.W. Kamp, S.A. Weitzman (Cancer Investigation, 1996).

The study

• Authors: B.T. Mossman, D.W. Kamp, S.A. Weitzman
• Journal: Cancer Investigation
• Published: 1996;14(5):466-80
• Type of article: Review
• Cited by: 145 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Exposure to asbestos, particularly members of the amphibole subgroup (crocidolite, amosite), is associated with the development of malignant mesothelioma and lung cancer. Although management of asbestos in buildings and increased regulation of asbestos in workplace settings are viable approaches to the prevention of disease, the prognosis of asbestos-associated tumors is generally dismal. Moreover, although a vast amount of information is available on the responses of cells and tissues to fibers, understanding the pathogenesis of asbestos-associated malignancies is hampered by the complexity of and differences between various fiber types. Multiple interactions between components of cigarette smoke and asbestos may be important in the development of lung cancer. In this article, the general properties of asbestos fibers will be discussed with an emphasis on chemical and physical features implicated in tumorigenesis. We will then provide a brief overview of the clinical features and treatment of cancers associated with exposure to asbestos. Finally, we will review recent experimental data providing some insight into the cellular and molecular mechanisms of carcinogenesis by asbestos.

In plain English

This article was a review, not a new study. The authors summarized published research on asbestos fiber types, the clinical features and treatment of asbestos-associated cancers, and experimental evidence on how asbestos may cause cancer. They described two subgroups of asbestos: serpentine (chrysotile) and the more durable, rod-like amphiboles. Citing other studies, they reported three points about lung cancer: cigarette smoke generally increases lung cancer incidence in asbestos workers in a multiplicative manner; tumor location and tissue type cannot by themselves show what caused an individual's lung cancer; and whether asbestosis is a causal factor remained an open question. They reported that most patients with malignant pleural mesothelioma die within a year of diagnosis, and that no therapy had emerged as superior to supportive therapy alone. They noted that no candidate proto-oncogenes or tumor suppressor genes had been clearly associated with asbestos-associated lung cancers and mesothelioma. They described a prevention trial (CARET) that was stopped early after a 28% increase in lung cancer incidence in the treated group. The authors concluded that understanding the molecular mechanisms would permit new strategies for diagnosis, staging and therapy.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Narrative review of published clinical, epidemiological, animal and cell studies (no new data collected)
• Who was studied: Not a study of a single population; the review drew on published studies of asbestos workers, mesothelioma and lung cancer patients, rodents and cultured cells
• Exposure: Asbestos fibers: serpentine chrysotile and the amphiboles crocidolite, amosite, tremolite, anthophyllite and actinolite. The review also covered interactions with cigarette smoke and the role of fiber size.
• Main results:
  • The authors cited evidence that features of chrysotile may explain its relative lack of persistence in the lung over the long latency period of mesothelioma
  • Citing other studies, the authors stated that cigarette smoke generally increases bronchogenic carcinoma incidence in a multiplicative manner, compared with nonsmoking asbestos workers or with smokers without asbestos exposure
  • The authors stated that tumor location and histopathology are insufficient markers of causality in individual lung cancer patients
  • The authors stated that whether asbestosis is a causal factor in asbestos-related carcinomas of the respiratory tract remains an open question
  • Citing a published review of 20 studies, the authors reported that 15 of the studies found no relationship between pleural plaques and lung cancer risk
  • The authors reported that the majority of patients with malignant pleural mesothelioma die within a year of diagnosis, and that no therapy had emerged as superior to supportive therapy alone
  • The authors cited animal experiments pointing to the importance of long, thin fibers in inducing lung tumors and mesotheliomas
  • The authors cited laboratory studies in which asbestos fibers activated the proto-oncogenes c-fos and c-jun in rodent mesothelial and tracheal epithelial cells grown in the laboratory
  • The authors reported that, despite intense investigation, no candidate proto-oncogenes or tumor suppressor genes had been clearly associated with the development of asbestos-associated lung cancers and mesothelioma
  • The authors described the CARET trial of beta-carotene and retinyl palmitate in smokers and asbestos-exposed workers. They reported that it was stopped early because of a 28% increase in lung cancer incidence in the experimental group.
• The authors' conclusion: The authors concluded that the effects of asbestos, particularly iron-containing amphibole fibers, may be mediated through oxidant-dependent mechanisms. They also concluded that elucidating the molecular mechanisms of asbestos-induced cancers will permit new strategies for diagnosis, staging and therapy.
• Limitations the authors state:
  • The authors cautioned that fiber analyses of lungs or tumors at autopsy reflect patterns after disease develops and cannot by themselves show what caused the disease

Topics

The National Library of Medicine indexes this study under subjects our site covers: Lung cancer, Mesothelioma.

Medical terms in this study, explained in our Lexicon: Carcinogenesis, Amphibole Group, Crocidolite, Amosite, Mesothelioma, Lung Cancer, Prognosis.

Related studies

• Mechanisms of asbestos carcinogenesis — B.T. Mossman, J.E. Craighead (1981)
• Mechanisms of asbestos carcinogenesis and toxicity: the amphibole hypothesis revisited — B.T. Mossman (1993)
• Asbestosis: clinical spectrum and pathogenic mechanisms — D.W. Kamp, S.A. Weitzman (1997)
• Pulmonary oxidative stress, inflammation and cancer: respirable particulate matter, fibrous dusts and ozone as major causes of lung carcinogenesis through reactive oxygen species mechanisms — A. Valavanidis, T. Vlachogianni, et al. (2013)
• Tobacco smoke: involvement of reactive oxygen species and stable free radicals in mechanisms of oxidative damage, carcinogenesis and synergistic effects with other respirable particles — A. Valavanidis, T. Vlachogianni, et al. (2009)
• Molecular pathways: targeting mechanisms of asbestos and erionite carcinogenesis in mesothelioma — M. Carbone, H. Yang (2012)

Browse more research in Cancer Investigation, or return to medical research.