Identification of a common microdeletion cluster in 7q21.3 subband among patients with myeloid leukemia and myelodysplastic syndrome

Biochemical and Biophysical Research Communications Volume 383 Issue 2 Page 245-251 published_at 2009
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Title ( eng )
Identification of a common microdeletion cluster in 7q21.3 subband among patients with myeloid leukemia and myelodysplastic syndrome
Creator
Asou Hiroya
Ozaki Yuko
Nakamura Megumi
Aki Daisuke
Source Title
Biochemical and Biophysical Research Communications
Volume 383
Issue 2
Start Page 245
End Page 251
Abstract
Monosomy 7 and interstitial deletions in the long arm of chromosome 7 (-7/7q-) is a common non-random chromosomal abnormality found frequently in rnyeloid disorders including acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and juvenile myelomonocytic leukemia (JMML). Using a short probe-based microarray comparative genomic hybridization (mCGH) technology, we identified a common microdeletion Cluster in 7q21.3 subband, which is adjacent to 'hot deletion region' thus far identified by conventional methods. This common microdeletion cluster contains three poorly characterized genes; Samd9, Samd9L, and a putative gene LOC253012, which we named Miki. Gene copy number assessment of three genes by real-time PCR revealed heterozygous deletion of these three genes in adult patients with AML and MDS at high frequency, in addition to JMML patients. Miki locates to mitotic spindles and centrosomes and downregulation of Miki by RNA interference induced abnormalities in mitosis and nuclear morphology, similar to myelodysplasia. In addition, a recent report indicated Samd9 as a tumor suppressor. These findings indicate the usefulness of the short probe-based CGH to detect microdeletions. The three genes located to 7q21.3 would be candidates for myeloid tumor-suppressor genes on 7q.
Keywords
Monosomy
Myeloid malignancy
Tumor suppressor
Mitosis
NDC
Medical sciences [ 490 ]
Language
eng
Resource Type journal article
Publisher
Academic Press Inc
Elsevier Science
Date of Issued 2009
Rights
Copyright (c) 2009 Elsevier Inc.
Publish Type Author’s Original
Access Rights open access
Source Identifier
[ISSN] 0006-291X
[DOI] 10.1016/j.bbrc.2009.04.004
[NCID] AA00564395
[DOI] http://dx.doi.org/10.1016/j.bbrc.2009.04.004