| Literature DB >> 20015882 |
Frank Stegelmann1, Lars Bullinger, Martin Griesshammer, Karlheinz Holzmann, Marianne Habdank, Susanne Kuhn, Carmen Maile, Stefanie Schauer, Hartmut Döhner, Konstanze Döhner.
Abstract
Single-nucleotide polymorphism arrays allow for genome-wide profiling of copy-number alterations and copy-neutral runs of homozygosity at high resolution. To identify novel genetic lesions in myeloproliferative neoplasms, a large series of 151 clinically well characterized patients was analyzed in our study. Copy-number alterations were rare in essential thrombocythemia and polycythemia vera. In contrast, approximately one third of myelofibrosis patients exhibited small genomic losses (less than 5 Mb). In 2 secondary myelofibrosis cases the tumor suppressor gene NF1 in 17q11.2 was affected. Sequencing analyses revealed a mutation in the remaining NF1 allele of one patient. In terms of copy-neutral aberrations, no chromosomes other than 9p were recurrently affected. In conclusion, novel genomic aberrations were identified in our study, in particular in patients with myelofibrosis. Further analyses on single-gene level are necessary to uncover the mechanisms that are involved in the pathogenesis of myeloproliferative neoplasms.Entities:
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Year: 2009 PMID: 20015882 PMCID: PMC2857198 DOI: 10.3324/haematol.2009.013623
Source DB: PubMed Journal: Haematologica ISSN: 0390-6078 Impact factor: 9.941