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127. Kongress der Deutschen Gesellschaft für Chirurgie

Deutsche Gesellschaft für Chirurgie

20.04. - 23.04.2010, Berlin

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Serum midkine correlates with tumor progression and imatinib response in gastrointestinal stromal tumors

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  • Tamina Rawnaq - Universitätsklinikum Hamburg-Eppendorf, Allgemein-, Viszeral- und Thoraxchirurgie, Hamburg, Deutschland
  • Miriam Kunkel - Universitätsklinikum Hamburg-Eppendorf, Allgemein-, Viszeral- und Thoraxchirurgie, Hamburg, Deutschland
  • Ronald Simon - Universitätsklinikum Hamburg-Eppendorf, Institut für Pathologie, Hamburg, Deutschland
  • Hilke Zander - Universitätsklinikum Hamburg-Eppendorf, Klinik und Poliklinik für Allgemein-, Viszeral- und Thoraxchirurgie, Hamburg, Deutschland
  • Kai Bachmann - Universitätsklinikum Hamburg-Eppendorf, Allgemein-, Viszeral- und Thoraxchirurgie, Hamburg, Deutschland
  • Guido Sauter - Universitätsklinikum Hamburg-Eppendorf, Pathologie, Hamburg, Deutschland
  • Jakob R. Izbicki - Universitätsklinikum Hamburg-Eppendorf, Klinik und Poliklinik für Allgemein-, Viszeral- und Thoraxchirurgie, Hamburg, Deutschland
  • Jussuf T. Kaifi - Universitätsklinikum Hamburg-Eppendorf, Klinik und Poliklinik für Allgemein-, Viszeral- und Thoraxchirurgie, Hamburg, Deutschland

Deutsche Gesellschaft für Chirurgie. 127. Kongress der Deutschen Gesellschaft für Chirurgie. Berlin, 20.-23.04.2010. Düsseldorf: German Medical Science GMS Publishing House; 2010. Doc10dgch237

doi: 10.3205/10dgch237, urn:nbn:de:0183-10dgch2377

Published: May 17, 2010

© 2010 Rawnaq et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

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Introduction: A previous study identified midkine (MK) expression in primary gastrointestinal stromal tumor (GIST) as a prognostic marker. The aim of the current study was to compare serum midkine (S-MK) concentrations of GIST patients with those of healthy controls and to determine if MK can serve as a prognostic serum marker for these patients.

Materials and methods: S-MK concentrations were measured by enzyme-linked immunosorbent assay in GIST patients (n=96) and healthy controls (n=148). S-MK levels were then correlated with clinicopathological data and the administration of imatinib therapy. In addition, MK expression was evaluated in 39 surgically resected GIST and in 17 leiomyoma specimens on a tissue microarray.

Results: S-MK concentrations in GIST patients were significantly higher than in healthy controls: median (25th and 75th percentiles) S-MK concentration was 235 (139 and 376) pg/ml in the GIST patients and 99 (33 and 198) pg/ml in the controls (p<0.001; Mann-Whitney U test). Significantly higher median S-MK concentrations were found in GIST with recurrence compared to those without (295 vs. 230; p=0.009). GIST patients with S-MK levels over 400 pg/ml showed a significantly worse recurrence-free survival (p=0.026; log-rank test). Patients receiving imatinib therapy had decreased median S-MK concentrations in comparison to those who were not treated with imatinib (331 vs. 201; p<0.001).

Conclusion: S-MK concentration is a potential marker for evaluating the progression and prognosis of GIST, especially during imatinib therapy. Further studies could focus on the role of midkine in the tumorigenesis of GIST and responsiveness toward imatinib therapy.