Genomic imbalances including amplification of the tyrosine kinase gene JAK2 in CD30+ Hodgkin cells

Cancer Res. 2000 Feb 1;60(3):549-52.

Abstract

Comparative genomic hybridization was applied for a comprehensive screening of frequently occurring net gains and losses of chromosomal subregions in small populations of CD30+ Hodgkin cells and their morphological variants. In 12 Hodgkin's lymphomas, recurrent gains were detected on chromosomal arms 2p, 9p, and 12q (in six, four, and five tumors, respectively) and distinct high-level amplifications were identified on chromosomal bands 4p16, 4q23-q24, and 9p23-p24. In Hodgkin cells with 9p23-p24 amplification, fluorescence in situ hybridization revealed an increased copy number of chromosomal sequences spanning the tyrosine kinase gene JAK2. Several of the imbalances described, in particular a gain in chromosomal arm 9p that includes JAK2 amplification, are similar to the genomic changes detected in primary mediastinal B-cell lymphoma.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Chromosome Aberrations*
  • Female
  • Gene Dosage
  • Hodgkin Disease / genetics*
  • Humans
  • Janus Kinase 2
  • Ki-1 Antigen / analysis*
  • Male
  • Middle Aged
  • Nucleic Acid Hybridization
  • Protein-Tyrosine Kinases / genetics*
  • Proto-Oncogene Proteins*

Substances

  • Ki-1 Antigen
  • Proto-Oncogene Proteins
  • Protein-Tyrosine Kinases
  • JAK2 protein, human
  • Janus Kinase 2