Nuclear receptor co-repressor gene localizes to 17p11.2, a frequently deleted band in malignant disorders

The t(8;21) between the AML1 and ETO genes is a commonly seen genetic alteration in acute myeloid leukemia. Recently, we reported that the fusion partner ETO binds to the human nuclear receptor co‐repressor (NCOR), a member of the NCOR/SIN3/histone deacetylase complex. This complex mediates transcri...

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Veröffentlicht in:Genes chromosomes & cancer 1999-06, Vol.25 (2), p.191-193
Hauptverfasser: Stacey, Michael W., Wang, Jianxiang, Byrd, Rebecca L., Liu, Johnson M., Kearns, William G.
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Sprache:eng
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Zusammenfassung:The t(8;21) between the AML1 and ETO genes is a commonly seen genetic alteration in acute myeloid leukemia. Recently, we reported that the fusion partner ETO binds to the human nuclear receptor co‐repressor (NCOR), a member of the NCOR/SIN3/histone deacetylase complex. This complex mediates transcriptional repression as a result of chromatin remodeling. Here, we used a combination of fluorescence in situ hybridization and hybrid panels to localize the human NCOR gene (NCOR) to chromosome band 17p11.2. The position of human NCOR on 17p11 raises the possibility of deranged transcriptional regulation in malignant disorders associated with deletions of 17p. Genes Chromosomes Cancer 25:191–193, 1999. Published 1999 Wiley‐Liss, Inc.
ISSN:1045-2257
1098-2264
DOI:10.1002/(SICI)1098-2264(199906)25:2<191::AID-GCC16>3.0.CO;2-8