1. ¹National Research Centre for Asbestos Related Diseases, Western Australian Institute of Medical Research, University of Western Australia, Perth, Western Australia, Australia
2. ²Australian Mesothelioma Tissue Bank, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia
3. ³Department of Anatomical Pathology, PathWest, Queen Elizabeth II Medical Centre, Perth, Western Australia, Australia
4. ⁴Department of Pathology, University of Western Australia, Perth, Western Australia, Australia
5. ⁵PathWest, Queen Elizabeth II Medical Centre, Perth, Western Australia, Australia
6. ⁶PathWest Department of Cytogenetics, PathWest, King Edward Memorial Hospital, Perth, Western Australia, Australia
7. ⁷Department of Pediatrics, University of Adelaide, Adelaide, Australia
8. ⁸School of Surgery and Pathology, University of Western Australia, Perth, Western Australia, Australia
9. ⁹School of Medicine and Pharmacology, University of Western Australia, Perth, Western Australia, Australia
10. ¹⁰Department of Medical Oncology, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia
11. ¹¹Department of Respiratory Medicine, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia

Correspondence: Dr J Creaney, School of Medicine and Pharmacology, University of Western Australia, 4th Floor, G block, QE2MC, Verdun St, Nedlands, WA 6009, Australia. E-mail: creaneyj@cyllene.uwa.edu.au

Received 10 October 2007; Revised 4 March 2008; Accepted 10 March 2008; Published online 29 April 2008.

Abstract

Current interest in the MUC1/EMA mucin relates to its role in malignancy, and its potential as a therapeutic target. MUC1/EMA expression has been observed in the majority of epithelioid mesotheliomas. However, little is known of the characteristics of MUC1/EMA in mesothelioma. Herein, we studied the cell surface and soluble expression of the MUC1/EMA glycoprotein, and determined the mRNA and genomic expression profiles in mesothelioma. We found that the anti-MUC1 antibody, E29, was the most diagnostically useful of seven antibody clones examined with a sensitivity of 84% (16 out of 19 cases) and no false positive results. MUC1 mRNA expression was significantly higher in mesothelioma samples than in benign mesothelial cells. No amplification of the MUC1 gene was observed by FISH. Seven of 9 mesothelioma samples expressed MUC1-secreted mRNA isoform in addition to the archetypal MUC1/transmembrane form. CA15.3 (soluble MUC1) levels were significantly higher in the serum of mesothelioma patients than in healthy controls but were not significantly different to levels in patients with benign asbestos-related disease. CA15-3 in effusions could differentiate malignant from benign effusions but were not specific for mesothelioma. Thus, as in other cancers, alterations in MUC1 biology occur in mesothelioma and these results suggest that specific MUC1 characteristics may be useful for mesothelioma diagnosis and should also be investigated as a potential therapeutic target.