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Gain of chromosome 6p is an infrequent cause of increased PIM1 expression in B-cell non-Hodgkin's lymphomas

Leukemia volume 20, pages 539–542 (2006)Cite this article

Gains and losses of genomic material are changes that play central roles in tumor development and progression. Comparative genomic hybridization (CGH) allows for the detection of over- and underrepresented sequences in tumor DNA as compared to normal DNA, and such genomic aberrations have been shown to have prognostic value in several studies of primary lymphomas. The serine/threonine kinase PIM1 is a known oncogene that has previously been shown to be upregulated in prostate cancer. Overexpression of PIM1 in cell lines protects against apoptosis induced by genotoxic agents. The PIM1 gene is localized to chromosome 6p21.2. Parts of chromosome 6 or the whole 6p arm are gained in a subset of B-cell non-Hodgkin's lymphomas, and these gains are associated with a poor prognosis.1

Dual color interphase FISH studies showed that there were two copies of centromere 6 in both Reh and U698 cells. In contrast, U698 exhibited one normal signal and in addition a cluster of 15–20 signals from the PIM1 probe (RP3-355M6), probably representing intrachromosomal amplification of the PIM1 gene (Supplementary Figure 1). Translocations in lymphomas targeting CCND3 has been described, and high BMP6 expression has been shown to be of negative prognostic value in DLBCL.4 Considering these genes as possible targets for chromosomal alterations, we performed FISH with a probe for CCND3 (RP5-973N23), located at 6p21 and BMP6 (RP1-119C5) located at 6p24. Whereas there were only two signals from the BMP6 probe, the CCND3 probe generated four signals, indicating that this gene is also represented in a proportion of the amplica in U698 cells.

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Acknowledgements

The Norwegian Cancer Society and The Norwegian Research Council supported this work.

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Authors and Affiliations

  1. Department of Immunology, Institute of Cancer Research, Health Enterprise Rikshospitalet-Radiumhospitalet, Oslo, Norway

    E A Sivertsen, S Patzke & E B Smeland

  2. Department of Radiation Biology, Institute of Cancer Research, Health Enterprise Rikshospitalet-Radiumhospitalet, Oslo, Norway

    E Galteland & T Stokke

  3. Cold Spring Harbor Laboratory, Genome Research Center, Woodbury, NY, USA

    D Mu

  4. Department of Oncology, Institute of Cancer Research, Health Enterprise Rikshospitalet-Radiumhospitalet, Oslo, Norway

    H Holte

  5. Department of Tumor Biology, Institute of Cancer Research, Health Enterprise Rikshospitalet-Radiumhospitalet, Oslo, Norway

    L Meza-Zepeda & O Myklebost

  6. Faculty Division, The Norwegian Radium Hospital, Oslo, Norway

    E B Smeland

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  1. E A Sivertsen
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Correspondence to T Stokke.

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Supplementary Information accompanies the paper on the Leukemia website (http://www.nature.com/leu)

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Sivertsen, E., Galteland, E., Mu, D. et al. Gain of chromosome 6p is an infrequent cause of increased PIM1 expression in B-cell non-Hodgkin's lymphomas. Leukemia 20, 539–542 (2006). https://doi.org/10.1038/sj.leu.2404094

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