Pulmonary adenocarcinoma with epidermal growth factor receptor-mutations in asbestos exposed non-smokers: A case series

Our plain-English summary of Pulmonary adenocarcinoma with epidermal growth factor receptor-mutations in asbestos exposed non-smokers: A case series, by R.L. Kradin, J. Iafrate, D.C. Christiani (American Journal of Industrial Medicine, 2017).

The study

• Authors: R.L. Kradin, J. Iafrate, D.C. Christiani
• Journal: American Journal of Industrial Medicine
• Published: 2017;60(3):306-309
• Type of article: Case report
• Cited by: 1 article, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Background: Cigarette smoke and asbestos are recognized causes of lung carcinoma and together promote carcinogenesis. Adenocarcinoma is currently the most common cause of lung cancer in the USA and it has been linked to both smoking and asbestos exposure. Mutations in the epidermal growth factor gene receptor (EGFR) occur predominantly in non-smokers with adenocarcinoma. Methods Mutations in the EGFR gene were investigated using next-generation sequencing.

Results: We report the presence of EGFR exon point mutations in the pulmonary adenocarcinomas of three never-smokers occupationally exposed to asbestos.

Conclusion: The role of asbestos as a possible cause of EGFR mutagenesis requires further investigation. Am. J. Ind. Med. 60:306-309, 2017. © 2017 Wiley Periodicals, Inc.

© 2017 Wiley Periodicals, Inc.

In plain English

This article was a case series about three men, aged 62 to 76, with lung adenocarcinoma who had never smoked and had worked around asbestos. They were referred to the authors for review. Their asbestos exposure was confirmed by their own history, social security records and sworn testimony by co-workers. One was a plumber from 1957 to 1979 who cut crocidolite-containing asbestos cement pipe. One had bystander exposure at a shipyard from 1966 to 1971. One was a boat captain in the mid-1970s whose cargo included asbestos-containing drilling mud. The authors did not measure exposure levels. Testing found a change in the EGFR gene in every tumor: in exon 21 in two men, and an insertion mutation in exon 20 in the third. Two men had calcified pleural plaques. None had X-ray signs of asbestosis. The authors stated that they made no claim that asbestos caused these mutations. They called the series small, retrospective and uncontrolled, and said the findings raise a possibility that needs further controlled study.

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: Small retrospective, uncontrolled case series (three patients)
• Who was studied: Three men (aged 76, 69 and 62) with pulmonary adenocarcinoma who were lifelong non-smokers with occupational asbestos exposure. They were referred for review; the work was performed at Massachusetts General Hospital, but the patients were not seen primarily there. Exposure was confirmed by history, social security records and sworn co-worker testimony.
• Exposure: Case 1: plumber 1957 to 1979 who worked with asbestos-containing pipe, gasket and boiler insulation, cut crocidolite-containing asbestos cement pipe, and had childhood exposure from his father's dusty work clothes. Case 2: bystander exposure aboard vessels at a shipyard 1966 to 1971 (cutting of asbestos board and insulation, mixing of asbestos cement). Case 3: marine captain in the mid-1970s carrying sacks of asbestos-containing drilling mud, plus bystander exposure to pipe insulation in engine rooms. The authors assumed all three were exposed to both chrysotile and amphibole asbestos. Exposures were not quantified.
• Main results:
  • Case 1 (76-year-old plumber): metastatic pulmonary adenocarcinoma with bilateral calcified pleural plaques. Molecular analysis showed an insertion mutation at exon 20 of the EGFR gene.
  • Case 2 (69-year-old shipyard worker): adenocarcinoma with calcified bilateral pleural plaques. The tumor had an EGFR mutation at exon 21, and there was no histological evidence of asbestosis or asbestos bodies by light microscopy.
  • Case 3 (62-year-old marine captain): 3.0 cm right upper lobe adenocarcinoma with a mutation in exon 21 of the EGFR gene.
  • Two of the three men had calcified pleural plaques on imaging. None of the three had radiographic evidence of pulmonary asbestosis.
• The authors' conclusion: The authors stated that they make no claims that asbestos caused the EGFR mutations. They said that finding EGFR mutations in never-smokers raises the possibility that asbestos may play a role, and that interpretation must be cautious. They concluded that further controlled investigations are warranted.
• Limitations the authors state:
  • Small, retrospective, uncontrolled case series, partly because it was difficult to find people who met all the study conditions
  • Asbestos exposures were not quantified
  • The frequency of EGFR mutations in people exposed to both cigarette smoke and asbestos has not been determined

Topics

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

Medical terms in this study, explained in our Lexicon: Adenocarcinoma, Carcinoma, Carcinogenesis, Lung Cancer, Asbestos Exposure, EGFR, Next-Generation Sequencing (NGS).

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