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Chromosome 11q deletion in myeloid malignancies

Leukemia volume 16, pages 953–955 (2002)Cite this article

Chromosomal deletions are recurrent abnormalities in leukemia, implicating the loss of tumor suppressor genes as a significant mechanism in leukemogenesis. Deletion of long arms of chromosomes 5 and 7, moreover, predicts for a very poor prognosis in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).1,2 More recently, characterized deletions in myeloid malignancies include deletion 9q in AML,3 and deletion 20q in myeloproliferative disorder.4 Deletion 11q is a rare cytogenetic abnormality in the myeloid dis- orders, with a reported prevalence of 0.7% in de novo and secondary AML and MDS in one study.5 While the prognostic significance of del(11q) is uncertain, a previous report on deletion 11q23 showed that 15/16 AML and 5/12 MDS patients died with a median overall survival of 14.1 months.6 We performed molecular cytogenetics characterization of del(11q) abnormality based on archival material in AML and MDS patients diagnosed at our center. Fluorescence in situ hybridization (FISH) and comparative genomic hybridization (CGH) procedures were carried out in accordance with previously published protocols.7

As the mixed lineage leukemia (MLL) gene is located at the 11q23 breakpoint, we performed interphase FISH on six cases (1–3, 7–9) in which cells in Carnoy's fixative were available, using a MLL dual-color break-apart rearrangement probe (Vysis, Downers Grove, IL, USA). It consisted of a 350 kb centromeric fragment and a 190 kb telomeric fragment labeled with different fluorochromes. Four cases showed a predominance of a single fusion signal (Figure 1b), consistent with preservation of one allele and deletion of the other. Case 7 showed MLL split signal in keeping with gene rearrangement (Figure 1c), which was confirmed with Southern blot hybridization using PS/4 probe on BamHI, EcoRI and SacI digests (Figure 1d). Review of the karyotype showed subtle elongation of chromosome 6q (Figure 1e). Further metaphase FISH using the relevant whole chromosome painting probes (Vysis) showed addition of chromosome 11 material to 6q27 (Figure 1g), and was confirmed by employing respective painting probes with reversed fluorochrome label (data not shown). Unbalanced changes such as addition of chromosome 11qter material to the telomere of chromosome 6 was ruled out by the presence of intact telomeres on both chromosomes as demonstrated by FISH (Figure 1h) using a PNA telomere probe set (Dako, Copenhagen, Denmark). While chromosomal rearrangement in this case might have resulted in fusion between MLL and a candidate gene most likely AF6 based on breakpoint location at 6q27, unfortunately no sample was available to decipher this possibility. Finally, there was a predomi

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Acknowledgements

The study was supported by a CRCG grant of the University of Hong Kong.

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  1. Division of Hematology, Department of Pathology, The University of Hong Kong, Queen Mary Hospital, Hong Kong, People's Republic of China

    SK Ma, TSK Wan, LF Fung, CK So & LC Chan

  2. Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, People's Republic of China

    WY Au

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Ma, S., Wan, T., Au, W. et al. Chromosome 11q deletion in myeloid malignancies. Leukemia 16, 953–955 (2002). https://doi.org/10.1038/sj.leu.2402442

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