Gain of 1q21 and distinct adverse cytogenetic abnormalities correlate with increased microcirculation in multiple myeloma

Jens Hillengass, Christian M Zechmann, Andreas Nadler, Dirk Hose, Friedrich W Cremer, Anna Jauch, Christiane Heiss, Axel Benner, Anthony D Ho, Claus R Bartram, Hans-Ulrich Kauczor, Stefan Delorme, Hartmut Goldschmidt, Thomas M Moehler

Research output: Contribution to journalArticlepeer-review

19 Citations (Scopus)

Abstract

To identify genetic mechanisms controlling bone marrow microcirculation and angiogenesis in patients with plasma cell disease we simultaneously performed bone marrow dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) and cytogenetics (iFISH) on CD138 purified plasma cells of MGUS (n=31) and untreated multiple myeloma (MM) (n = 87) patients. The adverse cytogenetic abnormalities gain of 1q21, deletion 17p13 and deletion 13q14 significantly correlated with at least one DCE-MRI finding (aberrant "focal" microcirculation pattern, increase in median microcirculation parameter Amplitude A or exchange rate constant kep). We conclude that gain of 1q21, deletion 13q14 and deletion 17p13 trigger the angiogenic cascade in MM. Our findings will have important implications for the design, analysis and stratification for clinical studies of patients with MM in particular if compounds with antiangiogenic activity are used.

Original languageEnglish
Pages (from-to)2871-2875
Number of pages5
JournalInternational Journal of Cancer
Volume122
Issue number12
DOIs
Publication statusPublished - 15 Jun 2008
Externally publishedYes

Bibliographical note

(c) 2008 Wiley-Liss, Inc.

Keywords

  • Chromosome Aberrations
  • Chromosomes, Human, Pair 1
  • Female
  • Humans
  • In Situ Hybridization, Fluorescence
  • Magnetic Resonance Imaging
  • Male
  • Middle Aged
  • Multiple Myeloma/blood supply
  • Neovascularization, Pathologic/genetics

Fingerprint

Dive into the research topics of 'Gain of 1q21 and distinct adverse cytogenetic abnormalities correlate with increased microcirculation in multiple myeloma'. Together they form a unique fingerprint.

Cite this