p53 protein, EGF receptor, and anti-p53 antibodies in serum from patients with occupationally derived lung cancer.
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.
Schneider
J
J
Institut und Poliklinik für Arbeits- und Sozialmedizin, Justus-Liebig Universität Giessen, Germany.
Presek
P
P
Braun
A
A
Bauer
P
P
Konietzko
N
N
Wiesner
B
B
Woitowitz
H J
HJ
D000230:Adenocarcinoma / Q000097:blood / Q000209:etiology; D000368:Aged; D001323:Autoantibodies / Q000097:blood*; D014408:Biomarkers, Tumor / Q000097:blood*; D018287:Carcinoma, Large Cell / Q000097:blood / Q000209:etiology; D018288:Carcinoma, Small Cell / Q000097:blood / Q000209:etiology; D002294:Carcinoma, Squamous Cell / Q000097:blood / Q000209:etiology; D066246:ErbB Receptors / Q000097:blood*; D006801:Humans; D008171:Lung Diseases / Q000097:blood* / Q000209:etiology; D008175:Lung Neoplasms / Q000097:blood* / Q000209:etiology / Q000556:secondary; D008297:Male; D008654:Mesothelioma / Q000097:blood / Q000209:etiology; D008875:Middle Aged; D016273:Occupational Exposure; D010996:Pleural Effusion / Q000097:blood* / Q000209:etiology; D010997:Pleural Neoplasms / Q000097:blood / Q000209:etiology; D011658:Pulmonary Fibrosis / Q000097:blood / Q000209:etiology; D012016:Reference Values; D016159:Tumor Suppressor Protein p53 / Q000097:blood* / Q000276:immunology
D001323:Autoantibodies; D014408:Biomarkers, Tumor; D016159:Tumor Suppressor Protein p53; D066246:ErbB Receptors