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A potential role for PRDM12 in the pathogenesis of chronic myeloid leukaemia with derivative chromosome 9 deletion

Leukemia volume 18, pages 178–180 (2004)Cite this article

TO THE EDITOR

Chronic myeloid leukaemia (CML) is a clonal haematopoeic stem cell disorder associated with the BCR-ABL fusion gene, generated by the Philadelphia (Ph) translocation t(9;22)(q34;q11). Recently, it was established that deletions of over 300 kb occur on the derivative chromosome 9 [der(9)] in approximately 15% of CML patients.1 The deletions, detected by fluorescent in situ hybridisation (FISH) using large commercial contig probes, were associated with rapid progression to blast crisis and short survival. A recent study by Kolomietz et al2 used quantitative PCR to demonstrate that a further subset of der(9) deletions exist beyond the resolution of large commercial FISH probes. Subsequent mapping of the microdeletions identified a minimal commonly deleted region (CDR) of 120 kb, associated with short survival. The CDR, immediately 5′ to ABL, contained two known genes, the ribosomal RNA processing protein 4 (RRP4) and the positive regulatory (PR)-domain zinc-finger protein 12 (PRDM12). The latter gene is a member of the closely related PR-domain-containing zinc-finger family, which appear to function as negative regulators of oncogenesis and include the tumour-associated genes MDS1-EVI1, RIZ, BLIMP1, MEL1 and PFM1.3,4,5,6,7 PRDM12 therefore represents an attractive candidate tumour suppressor gene within the der(9) CDR.

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Acknowledgements

This work was supported by a generous grant from The Kay Kendall Leukaemia Fund. We are grateful to the Wellcome Trust Sanger Institute, Cambs, UK for providing chromosome 9 BAC clones.

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  1. Department of Academic Haematology, Molecular Cytogenetics Laboratory, Royal Free and University College Medical School, University College London, UK

    A G Reid & E P Nacheva

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Reid, A., Nacheva, E. A potential role for PRDM12 in the pathogenesis of chronic myeloid leukaemia with derivative chromosome 9 deletion. Leukemia 18, 178–180 (2004). https://doi.org/10.1038/sj.leu.2403162

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