p53 protein, EGF receptor, and anti-p53 antibodies in serum from patients with occupationally derived lung cancer

Our plain-English summary of p53 protein, EGF receptor, and anti-p53 antibodies in serum from patients with occupationally derived lung cancer, by J. Schneider, P. Presek, A. Braun, et al (British Journal of Cancer, 1999).

The study

• Authors: J. Schneider, P. Presek, A. Braun, P. Bauer, N. Konietzko, B. Wiesner, H.J. Woitowitz
• Journal: British Journal of Cancer
• Published: 1999;80(12):1987-94
• Cited by: 22 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

The oncogene product epidermal growth factor receptor (EGF-R), the tumour suppressor gene product p53 and anti-p53 antibodies are detectable in the serum of certain cancer patients. Increased levels of some of these products were reported in lung cancer patients after occupational asbestos exposure and after exposure to polycyclic aromatic hydrocarbons or vinylchloride. In the first step, this study investigated the possible diagnostic value of serum EGF-R, p53-protein and anti-p53 antibodies, measured by an enzyme-linked immunosorbent assay, in lung tumour patients. In addition to being investigated on a molecular epidemiological basis, these parameters were examined as biomarkers of carcinogenesis, especially with regard to asbestos incorporation effects or of radon-induced lung cancers. Also, a possible effect of cigarette smoking and age dependence were studied. A total of 116 male patients with lung or pleural tumours were examined. The histological classification was four small-cell cancers, six large-cell cancers, 32 adenocarcinomas, 47 squamous carcinomas, 12 mixed lung carcinomas, five diffuse malignant mesotheliomas and ten lung metastasis of extrapulmonary tumours. Twenty-two lung cancers and all mesotheliomas were related to asbestos, 22 lung cancers were related to ionizing radiation and 61 patients had cigarette smoke-related lung cancer. Besides these patients 50 male patients with non-malignant lung or pleural diseases were included; of the latter eight subjects suffered from asbestosis. Controls were 129 male subjects without any lung disease. No significantly elevated or decreased serum values for p53 protein, EGF-R, or anti-p53 antibodies as a function of histological tumour type, age, or degree and type of exposure (asbestos, smoking, ionizing radiation) could be found. The utility of p53-protein, EGF-R and anti-p53 antibodies as routine biomarkers for screening occupationally derived lung cancers is limited.

In plain English

This German multi-centre study measured three blood markers linked to cancer genes (p53 protein, the growth factor receptor EGF-R, and antibodies against p53) in 116 men with lung or pleural tumours, 50 with non-malignant lung or pleural disease and 129 without lung disease. The tumour patients included 22 with asbestos-related lung cancer, five with diffuse malignant pleural mesothelioma caused by asbestos dust, 61 with smoking-related lung cancer and 21 former uranium miners with radon-related lung cancer. Eight of the non-malignant patients had asbestosis. No significant differences in p53 protein or EGF-R were found between tumour patients, non-malignant disease patients and healthy controls. There were also no significant differences by tumour type, exposure, age or amount smoked. Anti-p53 antibodies appeared in 43 of 295 serum samples (14.6%), including 12% of healthy controls, with no significant group differences. The authors concluded that serum p53 protein does not appear useful as a marker for asbestos- or radon-induced lung cancer, and that EGF-R cannot be viewed as an early-effect marker for occupational diseases due to asbestos or for radon-induced lung cancer. They noted that some groups were small.

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: multi-centre study comparing serum levels of p53 protein, EGF-R and anti-p53 antibodies (measured by commercial ELISA kits) between patient groups and controls
• Who was studied: Men in Germany: 116 with lung or pleural tumours, 50 with non-malignant lung or pleural disease (26 with acute inflammatory infection, 24 with interstitial lung fibrosis) and 129 without lung disease; 295 serum samples in total
• Exposure: Occupational asbestos (fiber type not specified): 22 patients with asbestos-related lung cancer, 5 with diffuse malignant mesothelioma caused by asbestos dust and 8 with asbestosis. Ionizing radiation (radon and its decay products): 21 former uranium miners of SDAG Wismut with lung cancer. Cigarette smoking: 61 patients with smoking-related lung cancer. These groups were compared with 13 healthy never-smokers without known asbestos or radiation exposure.
• Main results:
  • Serum p53 protein and EGF-R concentrations did not differ significantly between tumour patients and patients with non-malignant lung disease or healthy controls.
  • Anti-p53 antibodies were detected in 43 of 295 serum samples (14.6%).
  • Half of the small-cell carcinoma patients (2 of 4) had anti-p53 antibodies, the highest prevalence. Healthy controls and patients with non-malignant disease each had 12% positive. There were no significant differences between groups.
  • By exposure group (asbestos-related mesothelioma and lung cancer, radiation-related lung cancer, smoking-related lung cancer, asbestosis, non-asbestos fibrosis, compared with 13 non-exposed healthy non-smokers), there were no significant differences in p53 protein, EGF-R or anti-p53 antibodies.
  • A statistically significant overexpression of serum EGF-R was not found in any group.
  • Across all 295 samples, none of the three markers depended on age (correlation coefficients r = 0.06 for p53 and r = 0.05 for EGF-R).
  • Among 238 current or former smokers, p53 protein and EGF-R levels were not significantly correlated with pack-years (r = 0.0 and r = 0.11).
• The authors' conclusion: The authors concluded that serum p53 protein does not appear to be a useful biomarker for asbestos- or radon-induced lung cancer. They also concluded that, based on their results, EGF-R cannot be viewed as a marker for early effects of occupational diseases due to asbestos or for radon-induced lung cancer, and that routine use of these biomarkers for occupationally derived lung cancers cannot be recommended.
• Limitations the authors state:
  • The lack of differences by tumour type may be due to the small number of patients in some groups.
  • Asbestos-related disorders cannot be told apart clinically or pathologically from tumours or fibrosis arising from other causes, and the data do not allow this distinction.
  • The predictive value of anti-p53 antibodies, which were also found in people without clinical cancer, awaits a planned follow-up.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Lung cancer, Pleural plaques and thickening.

Medical terms in this study, explained in our Lexicon: Lung Cancer, Asbestos Exposure, Biomarker, Carcinogenesis, Histological Subtype, Adenocarcinoma, Carcinoma, Malignant Mesothelioma.

Related studies

• Serum levels of pantropic p53 protein and EGF-receptor, and detection of anti-p53 antibodies in former uranium miners (SDAG Wismut) — J. Schneider, P. Presek, et al. (1999)
• Gender comparisons in human lung cancer: analysis of p53 mutations, anti-p53 serum antibodies and C-erbB-2 expression — D.G. Guinee, W.D. Travis, et al. (1995)
• Serum ras (p21) as a marker for occupationally derived lung cancer? — J. Schneider, P. Presek, et al. (2000)
• Detection of serum p53 protein in lung cancer patients — J.C. Luo, R. Zehab, et al. (1994)
• Therapeutic antitumor efficacy of anti-epidermal growth factor receptor antibody, cetuximab, against malignant pleural mesothelioma — J. Kurai, H. Chikumi, et al. (2012)
• Increased serum concentrations of growth factor receptors and Neu in workers previously exposed to asbestos — N. Lahat, P. Froom, et al. (1999)

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