The online version of this article (doi:10.1186/1477-7819-10-264) contains supplementary material, which is available to authorized users.
This manuscript contains original material that has not been published or submitted to any other journal. The authors declare no competing interests.
SM and DZ designed the study, analysed the data and drafted the manuscript. SK carried out the LOH analysis. IK and FT carried out the molecular studies and helped to draft the manuscript. TB, KS and RK provided the pathologic specimen and helped to draft the manuscript. HN and AK helped to draft the manuscript. All authors read and approved the final manuscript.
Vasoactive intestinal polypeptide secreting tumors(VIPomas) are rare endocrine tumors of the pancreas with an estimated incidence of 0.1 per million per year. The molecular mechanisms that mediate development of VIPomas are poorly investigated and require definition.
A genome- and gene expression analysis of specimens of a primary pancreatic VIPoma with hepatic metastases was performed. The primary tumor, the metastases, the corresponding healthy tissue of the liver, and the pancreas were compared with each other using oligonucleotide microarrays and loss of heterozygosity (LOH).
The results revealed multiple LOH events and several differentially expressed genes. Our finding of LOH and downregulation was conspicuous in the microarray analysis for the mismatch repair gene MSH2 in the primary pancreatic VIPoma tumor, the hepatic metastasis but not in the corresponding healthy tissue. Further a strong overexpression of the chemokine CXCR4 was detected in the hepatic metastases compared to its pancreatic primary. With a review of the literature we describe the molecular insights of metastatic development in VIPoma.
In VIPoma, defects in the mismatch repair system especially in MSH2 may contribute to carcinogenesis, and increased CXCR4 may be associated with liver metastasis.
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