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

M W Stacey1, J Wang, R L Byrd

  • 1Center for Pediatric Research, Division of Medical Genetics, Children's Hospital of the King's Daughters and Eastern Virginia Medical School, Norfolk, USA.

Genes, Chromosomes & Cancer
|May 25, 1999
PubMed

Insights

Researchers located the human nuclear receptor co-repressor (NCOR) gene to chromosome 17p11.2. This finding is significant for understanding transcriptional regulation in cancers with 17p deletions, particularly acute myeloid leukemia.

Area of Science:

  • Genetics
  • Molecular Biology
  • Cancer Research

Background:

  • The t(8;21) genetic alteration involving AML1 and ETO genes is frequent in acute myeloid leukemia.
  • The ETO fusion partner interacts with the human nuclear receptor co-repressor (NCOR), part of a complex that represses transcription via chromatin remodeling.

Purpose of the Study:

  • To determine the chromosomal location of the human NCOR gene.
  • To investigate the implications of NCOR localization for transcriptional regulation in hematologic malignancies.

Main Methods:

  • Fluorescence in situ hybridization (FISH).
  • Hybrid panel analysis.

Main Results:

  • The human NCOR gene was localized to chromosome band 17p11.2.
  • This specific location suggests potential disruption of transcriptional regulation in disorders involving 17p deletions.

Conclusions:

  • The chromosomal position of NCOR on 17p11.2 is a critical finding.
  • This localization may explain altered gene expression in cancers characterized by 17p deletions, including certain types of acute myeloid leukemia.

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