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This Article Full Text Full Text (PDF) All Versions of this Article: jcp.2005.026435v1 59/7/764    most recent Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Add article to my folders Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Scattone, A Articles by Serio, G Search for Related Content PubMed PubMed Citation Articles by Scattone, A Articles by Serio, G Pubmed/NCBI databases Substance via MeSH Hazardous Substances DB ASBESTOS Medline Plus Health Information Mesothelioma Pleural Disorders

Comparative genomic hybridisation in malignant deciduoid mesothelioma

¹ Department of Pathology, Medical School, University of Bari, Bari, Italy
² Department of Surgery and Pathology, Medical School, University of Foggia, Foggia, Italy
³ Medical Genetics, De Bellis IRCCS Hospital, Castellana Grotte (Bari), Bari
⁴ Department of Internal Medicine and Public Medicine, Industrial Medicine, Medical School, University of Bari
⁵ Department of Clinical Methodology, Medical School, University of Bari

Correspondence to:
Dr G Serio
Department of Pathology, Medical School, University of Bari, 11 G Cesare Square, 70124 Bari, Italy; g.serio{at}anatopat.uniba.it Background: Malignant deciduoid mesothelioma is a rare variant of epithelioid mesothelioma. This tumour generally has poor prognosis, and can be asbestos related.

Aim: To identify peculiar genetic changes responsible for critical phases in pathogenesis of malignant deciduoid mesothelioma and their prognostic relevance.

Methods: Comparative genomic hybridisation was carried out in six cases of malignant pleural deciduoid mesothelioma, four sporadic and two familial. All cases were found to be asbestos related. Four patients died during follow-up and the mean survival was 29.5 (SD 14.2, range 12–43) months.

Results: Genetic abnormalities were found in all the tumour tissues, the most frequent being chromosomal gains at 1p, 12q, 17, 8q, 19 and 20 and losses at 13q, 6q and 9p. Survival was found to be longer in those patients who presented a smaller number of losses (2) in the tumorous chromosomes.

Conclusions: Although numerous genetic changes are presented by deciduoid mesotheliomas, certain chromosomal regions are preferentially affected. The clinical outcome for this mesothelioma subtype is predicted by the number of losses.

Abbreviations: CGH, comparative genomic hybridisation