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Blood, 15 April 2006, Vol. 107, No. 8, pp. 3389-3396.
Prepublished online as a Blood First Edition Paper on December 20, 2005; DOI 10.1182/blood-2005-08-3431.
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Submitted August 24, 2005
Accepted December 7, 2005
Frequent genomic alterations in epithelium measured by microsatellite instability following allogeneic hematopoietic cell transplantation in humans
Philipp Faber, Paul Fisch, Miguel Waterhouse, Annette Schmitt-Graff, Hartmut Bertz, Jurgen Finke, and Alexandros Spyridonidis*
Department of Hematology / Oncology, Albert Ludwigs University of Freiburg, Freiburg, Germany
Department of Pathology, Albert Ludwigs University of Freiburg, Freiburg, Germany
* Corresponding author; email: spyridonidis{at}mm11.ukl.uni-freiburg.de.
While typically found in cancers, frameshift mutations in microsatellites have also been detected in chronically inflamed tissues. Allogeneic hematopoietic cell transplantation (HCT) may potentially produce chronic tissue stress through graft-versus-host reactions. We examined non-neoplastic epithelial tissues (colon, buccal) obtained 1 to 5061 days after human allogeneic HCT for the presence of genomic alterations at three tetranucleotide and three mononucleotide microsatellite loci. Novel bands indicative of microsatellite instability (MSI) at tetranucleotide repeats were detected in laser-microdissected colonic crypts and in buccal smears of 75% and 42% allografted patients, respectively. In contrast, no MSI was found in similar tissues from control subjects and from patients after intensive chemotherapy, nor in buccal cells from patients after autologous HCT. The MSI found in colon, which was often affected by graft-versus-host disease, was not due to loss of expression or nitrosylation of DNA repair proteins. MSI in clinically intact oral mucosa was more frequently found at later time points after HCT. MSI was also found in three post-transplant squamous cell cancers examined. Our data show that genomic alterations in epithelium regularly occur after allogeneic HCT and may be implicated in the evolution of post-transplant diseases, including secondary cancer.
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