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Updated: Jul 9, 2026
14:47
Identification of MyoD Interactome Using Tandem Affinity Purification Coupled to Mass Spectrometry
Published on: May 17, 2016
Alu elements mediate MYB gene tandem duplication in human T-ALL
Jennifer O'Neil1, Joelle Tchinda, Alejandro Gutierrez
1Department of Pediatric Oncology, Belfer Foundation Institute for Innovative Cancer Science, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
The Journal of Experimental Medicine
|December 12, 2007
Summary
The MYB oncogene is often duplicated in T cell acute lymphoblastic leukemia (T-ALL). This MYB duplication occurs through somatic homologous recombination, even in healthy individuals, and is selected during T-ALL development.
Area of Science:
- Genetics
- Oncology
- Molecular Biology
Background:
- The MYB oncogene plays a crucial role in cell proliferation and differentiation.
- MYB gene duplication is a frequent event observed in human T cell acute lymphoblastic leukemia (T-ALL).
Purpose of the Study:
- To investigate the mechanism of MYB oncogene duplication in T-ALL.
- To determine the frequency and potential role of MYB duplication in normal thymocyte development and T-ALL pathogenesis.
Main Methods:
- Analysis of the MYB locus structure in T-ALL.
- Nested long-range PCR to detect homologous recombination events.
- Investigation of MYB duplication in peripheral blood mononuclear cells of healthy individuals.
Main Results:
- The human MYB locus is flanked by Alu repeats, facilitating homologous recombination.
- MYB tandem duplication occurs via somatic homologous recombination between flanking Alu elements on sister chromatids.
- Low-frequency homologous recombination leading to MYB tandem duplication was detected in approximately 50% of healthy individuals, without germline duplication.
Conclusions:
- Alu-mediated MYB tandem duplication occurs at a low frequency during normal thymocyte development.
- This duplication event is clonally selected during the molecular pathogenesis of human T-ALL.
- The findings shed light on the mechanisms driving oncogene duplication in leukemia.
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