Blood Journal
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Prognostic and biologic significance of chromosomal imbalances assessed by comparative genomic hybridization in multiple myeloma

  1. Norma C. Gutiérrez,
  2. Juan L. García,
  3. Jesús M. Hernández,
  4. Eva Lumbreras,
  5. Mariana Castellanos,
  6. Ana Rasillo,
  7. Gema Mateo,
  8. José M. Hernández,
  9. Sonia Pérez,
  10. Alberto Orfao, and
  11. Jesús F. San Miguel
  1. From the Servicio de Hematología, Hospital Universitario de Salamanca, Salamanca, Spain; Centro de Investigación del Cáncer (CIC), Universidad de Salamanca-CSIC; and Servicio de Hematología, Hospital General de Segovia, Spain.

Abstract

Cytogenetic abnormalities, evaluated either by karyotype or by fluorescence in situ hybridization (FISH), are considered the most important prognostic factor in multiple myeloma (MM). However, there is no information about the prognostic impact of genomic changes detected by comparative genomic hybridization (CGH). We have analyzed the frequency and prognostic impact of genetic changes as detected by CGH and evaluated the relationship between these chromosomal imbalances and IGH translocation, analyzed by FISH, in 74 patients with newly diagnosed MM. Genomic changes were identified in 51 (69%) of the 74 MM patients. The most recurrent abnormalities among the cases with genomic changes were gains on chromosome regions 1q (45%), 5q (24%), 9q (24%), 11q (22%), 15q (22%), 3q (16%), and 7q (14%), while losses mainly involved chromosomes 13 (39%), 16q (18%), 6q (10%), and 8p (10%). Remarkably, the 6 patients with gains on 11q had IGH translocations. Multivariate analysis selected chromosomal losses, 11q gains, age, and type of treatment (conventional chemotherapy vs autologous transplantation) as independent parameters for predicting survival. Genomic losses retained the prognostic value irrespective of treatment approach. According to these results, losses of chromosomal material evaluated by CGH represent a powerful prognostic factor in MM patients. (Blood. 2004;104:2661-2666)

  • Submitted April 7, 2004.
  • Accepted June 13, 2004.
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