1. ¹Department of Dermatology and Allergy, Skin Cancer Center Charité, Charité – Universitätsmedizin Berlin, Berlin, Germany
2. ²Department of Dermatology, Università Cattolica del Sacro Cuore, Rome, Italy
3. ³Institute of Pathology, Charité – Universitätsmedizin Berlin, Berlin, Germany

Correspondence: Dr Chalid Assaf, Department of Dermatology, Venerology and Allergy, Skin Cancer Center Charité, Charité – Universitätsmedizin Berlin, Charitéplatz 1, Berlin 10117, Germany. E-mail: chalid.assaf@charite.de

Received 20 July 2006; Revised 7 December 2006; Accepted 20 December 2006; Published online 29 March 2007.

Abstract

Mutator phenotypes with microsatellite instability (MSI) correlated with defects in the mismatch repair system are characteristic for a subset of solid neoplasms, but are rare in non-Hodgkin lymphomas. In mismatch repair-deficient mice, however, mutator-type non-Hodgkin lymphomas are the most frequent tumors. To determine the role of MSI in mycosis fungoides, we compared the states of the eight dinucleotide microsatellite loci DXS418, DXS453, DXS556, DXS1060, D1S201, D6S260, D9S162, and D10S215 in tumor cells of 12 well-characterized patients at early- and advanced-stage diseases to matched healthy tissue. We did not find any MSI, although all but one patient had progressed to advanced-stage disease within the timeframe of the study. Concordantly, the expression of mismatch repair genes was normal. These results suggest that progressive accumulation of mutations as detected by MS analysis does not play a major role in the pathogenesis or in the progression of mycosis fungoides.