Biomarkers

Our medical research library holds 6 studies published in Biomarkers (1997–2016). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 6 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it.

About the journal

• Publisher: Tayor & Francis
• Published: 1996 to the present, England
• Language: English
• ISSN: 1354-750X (print), 1366-5804 (electronic)
• Its record in the NLM Catalog

2010s

• Immune response profiling of malignant pleural mesothelioma for diagnostic and prognostic biomarkers. J. Creaney, I.M. Dick, A.W. Musk, et al. 2016;21(6):551-61. PubMed · Publisher

  Abstract

  The asbestos induced cancer malignant mesothelioma (MM) is difficult to diagnose and has a poor prognosis. MM is an immunological cancer, therefore autoantibodies may be suitable biomarkers and associated with prognosis. We used Protoarray(®) microarrays to determine immune responses to 8798 antigens in 10 MM and 10 asbestos exposed controls and developed diagnostic panels using 17 antigens from this. The AUC of these panels were independently tested in these 10 MM patients and controls and in a validation group of 36 controls and 35 MM patients using luminex assays; none of the antigens identified were validated. Immune responses to RAB38 were associated with a better prognosis.

• Tumour necrosis factor-alpha gene polymorphisms in asbestos-induced diseases. S. Helmig, N. Aliahmadi, J. Schneider. 2010;15(5):400-9. PubMed · Publisher

  Abstract

  Background: Tumour necrosis factor (TNF)-alpha influences the pathogenesis of lung fibrosis and carcinogenesis in normal cells. Polymorphisms of this gene have been suggested to be associated with susceptibility to lung diseases.

  Methods: Association studies were performed in German subjects, using control subjects (n = 177), pulmonary fibrosis patients (n = 612) and bronchial carcinoma patients (n = 374).

  Results: Compared with a healthy (control) group, a significant result could be obtained for the asbestosis (patient) group (crude odds ratio (OR(crude)) = 1.57; 95% confidence interval (CI) 1.05-2.36; p = 0.03), especially with severe lung asbestosis (OR(crude) = 4.15; 95% CI 1.06-16.16; p = 0.04). A significant association was revealed when comparing asbestosis patients (OR(crude) = 4.08; 95% CI 1.53-10.54; p = 0.004 and OR(adjusted) = 3.89; 95% CI 1.49-10.17; p = 0.006) with asbestos-induced lung cancer patients.

  Conclusion: The results confirm the hypothesis that TNF-alpha polymorphisms are associated with asbestos-induced fibrotic or malignant lung diseases in Germans.

2000s

• Serum growth factors in asbestosis patients. Y. Li, A. Karjalainen, H. Koskinen, et al. 2009;14(1):61-6. PubMed · Publisher

  Abstract

  Various growth factors, including platelet-derived growth factor (PDGF) and transforming growth factor (TGF)-beta, have been implicated in the pathogenesis of asbestos-induced disease. PDGF and TGF-beta levels were determined by enzyme-linked immunosorbent assays in the banked serum samples of a cohort of workers with asbestosis, and the relationships of the growth factor levels to the subsequent development of cancer and to the radiographic severity and progression of asbestosis in the cohort were examined. Serum levels of PDGF and TGF-beta were found to be unrelated to the development of cancer, and serum levels of PDGF were found to be unrelated to the severity and progression of asbestosis. However, serum levels of TGF-beta were found to be statistically significantly related to disease severity (p = 0.01), increasing approximately 2.4-fold from ILO radiographic category 0 to category 3, and they were marginally related to disease progression (p = 0.07), in multivariate analysis controlling for other contributory factors including cumulative asbestos exposure. This suggests that serum TGF-beta may be a useful biomarker for asbestos-induced fibrotic disease.

• Clara cell protein (CC16) in serum and bronchoalveolar lavage fluid of subjects exposed to asbestos. M. Petrek, C. Hermans, V. Kolek, et al. 2002;7(1):58-67. PubMed · Publisher

  Abstract

  The Clara cell protein (CC16) is a small and readily diffusible protein of 16 kDa secreted by bronchiolar Clara cells in the distal airspaces. These epithelial cells are altered in several pulmonary pathological processes induced by various lung toxicants. In the search for a new biomarker of asbestos-induced lung impairment, we used a sensitive immunoassay to determine the levels of CC16 in bronchoalveolar fluid (BALF) and serum of subjects exposed to asbestos compared with a group of healthy controls. In the BALF of asbestos-exposed subjects there was an insignificant trend towards CC16 elevation compared with controls, with a (mean +/- SD of 0.81 +/- 0.65 mg l-1 for asbestos-exposed subjects (n = 23) versus 0.39 +/- 0.19 mg l-1 for controls (n = 11) (p = 0.09). In serum, CC16 concentration was significantly increased among asbestos-exposed subjects, with values of 27.2 +/- 24.0 micrograms l-1 for asbestos-exposed subjects (n = 34) versus 16.1 +/- 7.6 micrograms l-1 for controls (n = 34) (p = 0.01). Regarding the effects of smoking, there were significant differences between generally lower CC16 levels in serum and BALF (p = 0.05 and 0.001, respectively) of smokers compared with the higher levels in non-smokers. Serum CC16 levels positively correlated with those in BALF, which is consistent with a diffusional transfer of CC16 from the bronchoalveolar space into the serum. No association, however, emerged between the levels of CC16 in serum or BALF and either the duration of asbestos exposure or the severity of the lung impairment as assessed by chest X-ray. These findings suggest that exposure to asbestos elicits early changes in the local and, importantly, also the systemic levels of CC16. This pneumoprotein therefore appears as a promising non-invasive biomarker of asbestos-induced lung injury and occupational disease in both smoking and non-smoking exposed subjects.

1990s

• 8 Hydroxydeoxyguanosine as a biomarker of workplace exposures. M. Toraason. 1999;4(1):3-26. PubMed · Publisher

  Abstract

  To date, the 8-hydroxydeoxyguanosine (8OHdG) DNA adduct has been used as a biomarker in 11 occupational health studies examining the potential for ten different workplace exposures to cause oxidative DNA damage. Exposures examined include asbestos, azo-dyes, benzene, chromium, coal dust, glassworks, rubber manufacturing, styrene, toluene and environmental tobacco smoke (ETS). Experimental designs that applied 8OHdG as biomarker varied dramatically among the studies. For example, one study detected increased urinary excretion in retired workers with a history of exposure to mining dusts, while a study of workers exposed to benzene showed that the pattern of urinary excretion of 8OHdG varied over a 24h period following exposure. All but one study reported increased 8OHdG relative to controls, but in three cases the increases were not statistically significant. Only one study demonstrated a dose-response relationship between a chemical exposure (benzene) in the workplace and elevated 8OHdG. In most cases, exposure data were lacking and the elevated 8OHdG could only be considered to be associated with a generalized job category. Numerous animal and human studies have demonstrated an effect of tobacco smoke on 8OHdG, including a study of ETS in the workplace. In the majority of occupational studies, however, smoking was found not to be a confounding variable. 8OHdG levels tended to be higher in women than men as did the response to an occupational exposure and/or smoking. Two of three studies that stratified workers by age found it to be a confounder for the 8OHdG adduct, but the relationship between age and 8OHdG was non-linear. Only one study considered the impact of dietary supplements on 8OHdG levels in workers despite the fact that diet can have a marked effect on an individual's response to oxidative stress. It is premature to consider 8OHdG as biomarker that can be used for decision making or for regulatory purposes. Nonetheless, these studies demonstrate that with additional characterization of the role 8OHdG plays in the exposure-disease continuum it may well serve as a powerful biomonitoring toolin the future.

• CYP1A1 genetic polymorphisms, tobacco smoking and lung cancer risk in a French Caucasian population. C. Bouchardy, H. Wikman, S. Benhamou, et al. 1997;2(2):131-4. PubMed · Publisher

  Abstract

  The CYP1A1 gene encoding for an enzyme involved in the metabolic activation of important tobacco carcinogens could be implicated in smoking-induced lung cancer. Given the strong association between tobacco smoking and lung cancer, the effect of tobacco smoke exposure has to be taken into account when studying the potential association between lung cancer and CYP1A1 genotypes. The effect of two CYP1A1 genetic polymorphisms (Mspl and IIe-Val) on lung cancer risk were evaluated using peripheral blood DNA from 150 lung cancer patients and 171 controls. The Mspl sitepresent allele was found among 19.3% of both cases and controls and the variant allele Val among 6.7% of cases and 8.8% of controls. Lung cancer risks associated with the Mspl site-present allele (OR= 0.9; 95%Cl: 0.5-1.8) or with the Val allele (OR= 0.8; 95%Cl: 0.3-1.9) were not increased after adjustment for tobacco and asbestos exposures. These results persisted when analyses were stratified on smoking status, daily consumption of tobacco or duration of smoking. Similar findings were obtained when squamous cell or small cell carcinomas were studied separately. This study thus suggests a minor role for the known CYP1A1 gene polymorphisms in predisposition to lung cancer among Caucasian populations.

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