p53 and ras gene mutations in lung cancer: implications for smoking and occupational exposures

Our plain-English summary of p53 and ras gene mutations in lung cancer: implications for smoking and occupational exposures, by K. Husgafvel-Pursiainen, M. Ridanpää, S. Anttila, et al (Journal of Occupational and Environmental Medicine, 1995).

The study

• Authors: K. Husgafvel-Pursiainen, M. Ridanpää, S. Anttila, H. Vainio
• Journal: Journal of Occupational and Environmental Medicine
• Published: 1995;37(1):69-76
• Type of article: Review
• Cited by: 50 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

This paper reviews mutational activation of ras oncogenes and inactivation of the p53 tumor suppressor gene in human lung cancer. We discuss the frequency, type, and location of mutations in these genes in relation to known etiological factors for lung cancer. The most studied examples of these are exposure to tobacco smoke, and to radon and asbestos fibers at work. We summarize data from our laboratory on K-ras and p53 mutations in fresh tissue samples from patients with resected primary lung carcinoma whose smoking and occupational histories were known. Most of the tumors examined were histologically non-small cell carcinoma (NSCLC), mainly of the squamous cell carcinoma and adenocarcinoma types. We compare the prevalence and nature of mutations in the two histological types of NSCLC.

In plain English

This 1995 article by researchers at the Finnish Institute of Occupational Health was a review of studies on mutations in the K-ras and p53 genes in lung cancer, especially studies on smoking and some occupational exposures. It also summarized the authors' own laboratory data. In tumors from 99 Finnish lung cancer patients who were smokers or ex-smokers, the authors found 49 tumors with a p53 mutation and 19 with a K-ras mutation. The p53 gene was mutated in 58% of squamous cell carcinomas and 42% of adenocarcinomas. K-ras mutations occurred almost exclusively in adenocarcinoma. In an earlier study by the authors, asbestos fiber concentrations in patients' lungs were measured by electron microscopy. In that study, a high lung asbestos fiber concentration showed an elevated but not statistically significant association with K-ras mutation (OR 2.2; 90% CI 0.55 to 8.68). All heavily asbestos-exposed patients in that study were current or former smokers, and no significant independent role for asbestos could be shown. The authors concluded that this finding suggested an interaction between asbestos and smoking, part of which appears to involve K-ras mutations.

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: Review of published studies, combined with a summary of the authors' own laboratory data on K-ras and p53 mutations in resected lung tumors
• Who was studied: 99 Finnish Caucasian patients with resected primary lung carcinoma, all smokers or ex-smokers: 52 squamous cell carcinoma, 36 adenocarcinoma and 11 other cell types. Study dates were not given.
• Exposure: Tobacco smoking, measured in pack-years, and occupational exposures. In the authors' earlier study, asbestos exposure was assessed as the asbestos fiber concentration in the lung, measured by electron microscopy. Fiber types were not named.
• Main results:
  • Among tumors from the 99 smokers, 49 tumors had a p53 mutation and 19 had a K-ras mutation
  • The p53 gene was mutated in 58% of squamous cell carcinoma tumors
  • The p53 gene was mutated in 42% of adenocarcinoma tumors
  • K-ras mutations occurred almost exclusively in adenocarcinoma
  • Adenocarcinoma patients with G to T substitutions in K-ras had smoked on average 52 pack-years; those with G to T transversions in p53 had smoked on average 34 pack-years
  • In the authors' earlier study, an elevated but nonsignificant association was found between high pulmonary asbestos fiber concentration and the presence of K-ras mutation (OR 2.2; 90% CI 0.55 to 8.68)
• The authors' conclusion: The authors concluded that the asbestos finding suggested an interaction between asbestos and smoking in tumor development, part of which appears to involve K-ras mutations
• Limitations the authors state:
  • All heavily asbestos-exposed patients were current or former smokers, so no significant independent role for asbestos could be demonstrated

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: Lung Cancer, Occupational Exposure, Tumor Suppressor Gene, Carcinoma, Squamous Cell Carcinoma, Adenocarcinoma.

Related studies

• Lung cancer and past occupational exposure to asbestos. Role of p53 and K-ras mutations — K. Husgafvel-Pursiainen, A. Karjalainen, et al. (1999)
• Survival in operable non-small-cell lung cancer: role of p53 mutations, tobacco smoking and asbestos exposure — T. Sioris, K. Husgafvel-Pursiainen, et al. (2000)
• K-ras mutations in human adenocarcinoma of the lung: association with smoking and occupational exposure to asbestos — K. Husgafvel-Pursiainen, P. Hackman, et al. (1993)
• Analysis of K-ras and p53 mutations in mesotheliomas from humans and rats exposed to asbestos — Z. Ni, Y. Liu, et al. (2000)
• Interaction between smoking and asbestos in human lung adenocarcinoma: role of K-ras mutations — H. Vainio, K. Husgafvel-Pursiainen, et al. (1993)
• Absence of p53 mutations in malignant mesotheliomas — O. Mor, P. Yaron, et al. (1997)

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