Affiliations: Department of Pathology, VUMC – VU University Medical Centre, The Netherlands | IPATIMUP – Institute of Molecular Pathology and Immunology, University of Porto, Portugal | Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Braga, Portugal | Academic Unit of Pathology, School of Medicine, University of Leeds, UK | Department of Surgery, LUMC – Leiden University Medical Centre, The Netherlands | Faculty of Medicine of the University of Porto and Hospital S. João, Portugal
Abstract: Gastric cancer is one of the most frequent malignancies in the world. Nonetheless, the knowledge of the molecular events involved in the development of gastric carcinoma is far from complete. One of the hallmarks of gastric cancer is chromosomal instability resulting in abnormal DNA copy number changes throughout the genome. Mixed gastric carcinomas constitute a rare histological entity, containing the two main histological phenotypes (diffuse and intestinal). Very little is known about the underlying mechanisms of phenotypic divergence in these mixed tumours. To the best of our knowledge only E-Cadherin mutations were implicated so far in the divergence of these tumours and nothing is known about the involvement of chromosome copy number changes in the two divergent histological components. In this study, we compared the DNA copy number changes, in the two different components (diffuse and intestinal) of mixed gastric carcinomas by microarray – comparative genomic hybridisation (array CGH). The analysis of 12 mixed gastric carcinomas showed no significant differences in array CGH profiles between the diffuse and intestinal components of mixed carcinomas. This supports the idea that the phenotypic divergence within mixed gastric carcinomas is not caused by DNA chromosomal aberrations.
