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RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia
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| Zeitschriftentitel: | International Journal of Molecular Sciences |
|---|---|
| Personen und Körperschaften: | , |
| In: | International Journal of Molecular Sciences, 20, 2019, 2, S. 350 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
MDPI AG
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| Schlagwörter: |
| author_facet |
van der Kouwe, Emiel Staber, Philipp van der Kouwe, Emiel Staber, Philipp |
|---|---|
| author |
van der Kouwe, Emiel Staber, Philipp |
| spellingShingle |
van der Kouwe, Emiel Staber, Philipp International Journal of Molecular Sciences RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia Inorganic Chemistry Organic Chemistry Physical and Theoretical Chemistry Computer Science Applications Spectroscopy Molecular Biology General Medicine Catalysis |
| author_sort |
van der kouwe, emiel |
| spelling |
van der Kouwe, Emiel Staber, Philipp 1422-0067 MDPI AG Inorganic Chemistry Organic Chemistry Physical and Theoretical Chemistry Computer Science Applications Spectroscopy Molecular Biology General Medicine Catalysis http://dx.doi.org/10.3390/ijms20020350 <jats:p>Oncogenic fusion protein RUNX1-ETO is the product of the t(8;21) translocation, responsible for the most common cytogenetic subtype of acute myeloid leukemia. RUNX1, a critical transcription factor in hematopoietic development, is fused with almost the entire ETO sequence with the ability to recruit a wide range of repressors. Past efforts in providing a comprehensive picture of the genome-wide localization and the target genes of RUNX1-ETO have been inconclusive in understanding the underlying mechanism by which it deregulates native RUNX1. In this review; we dissect the current data on the epigenetic impact of RUNX1 and RUNX1-ETO. Both share similarities however, in recent years, research focused on epigenetic factors to explain their differences. RUNX1-ETO impairs DNA repair mechanisms which compromises genomic stability and favors a mutator phenotype. Among an increasing pool of mutated factors, regulators of DNA methylation are frequently found in t(8;21) AML. Together with the alteration of both, histone markers and distal enhancer regulation, RUNX1-ETO might specifically disrupt normal chromatin structure. Epigenetic studies on the fusion protein uncovered new mechanisms contributing to leukemogenesis and hopefully will translate into clinical applications.</jats:p> RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia International Journal of Molecular Sciences |
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| title |
RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia |
| title_unstemmed |
RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia |
| title_full |
RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia |
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RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia |
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RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia |
| title_short |
RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia |
| title_sort |
runx1-eto: attacking the epigenome for genomic instable leukemia |
| topic |
Inorganic Chemistry Organic Chemistry Physical and Theoretical Chemistry Computer Science Applications Spectroscopy Molecular Biology General Medicine Catalysis |
| url |
http://dx.doi.org/10.3390/ijms20020350 |
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2019 |
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350 |
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<jats:p>Oncogenic fusion protein RUNX1-ETO is the product of the t(8;21) translocation, responsible for the most common cytogenetic subtype of acute myeloid leukemia. RUNX1, a critical transcription factor in hematopoietic development, is fused with almost the entire ETO sequence with the ability to recruit a wide range of repressors. Past efforts in providing a comprehensive picture of the genome-wide localization and the target genes of RUNX1-ETO have been inconclusive in understanding the underlying mechanism by which it deregulates native RUNX1. In this review; we dissect the current data on the epigenetic impact of RUNX1 and RUNX1-ETO. Both share similarities however, in recent years, research focused on epigenetic factors to explain their differences. RUNX1-ETO impairs DNA repair mechanisms which compromises genomic stability and favors a mutator phenotype. Among an increasing pool of mutated factors, regulators of DNA methylation are frequently found in t(8;21) AML. Together with the alteration of both, histone markers and distal enhancer regulation, RUNX1-ETO might specifically disrupt normal chromatin structure. Epigenetic studies on the fusion protein uncovered new mechanisms contributing to leukemogenesis and hopefully will translate into clinical applications.</jats:p> |
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| author | van der Kouwe, Emiel, Staber, Philipp |
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| description | <jats:p>Oncogenic fusion protein RUNX1-ETO is the product of the t(8;21) translocation, responsible for the most common cytogenetic subtype of acute myeloid leukemia. RUNX1, a critical transcription factor in hematopoietic development, is fused with almost the entire ETO sequence with the ability to recruit a wide range of repressors. Past efforts in providing a comprehensive picture of the genome-wide localization and the target genes of RUNX1-ETO have been inconclusive in understanding the underlying mechanism by which it deregulates native RUNX1. In this review; we dissect the current data on the epigenetic impact of RUNX1 and RUNX1-ETO. Both share similarities however, in recent years, research focused on epigenetic factors to explain their differences. RUNX1-ETO impairs DNA repair mechanisms which compromises genomic stability and favors a mutator phenotype. Among an increasing pool of mutated factors, regulators of DNA methylation are frequently found in t(8;21) AML. Together with the alteration of both, histone markers and distal enhancer regulation, RUNX1-ETO might specifically disrupt normal chromatin structure. Epigenetic studies on the fusion protein uncovered new mechanisms contributing to leukemogenesis and hopefully will translate into clinical applications.</jats:p> |
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| spelling | van der Kouwe, Emiel Staber, Philipp 1422-0067 MDPI AG Inorganic Chemistry Organic Chemistry Physical and Theoretical Chemistry Computer Science Applications Spectroscopy Molecular Biology General Medicine Catalysis http://dx.doi.org/10.3390/ijms20020350 <jats:p>Oncogenic fusion protein RUNX1-ETO is the product of the t(8;21) translocation, responsible for the most common cytogenetic subtype of acute myeloid leukemia. RUNX1, a critical transcription factor in hematopoietic development, is fused with almost the entire ETO sequence with the ability to recruit a wide range of repressors. Past efforts in providing a comprehensive picture of the genome-wide localization and the target genes of RUNX1-ETO have been inconclusive in understanding the underlying mechanism by which it deregulates native RUNX1. In this review; we dissect the current data on the epigenetic impact of RUNX1 and RUNX1-ETO. Both share similarities however, in recent years, research focused on epigenetic factors to explain their differences. RUNX1-ETO impairs DNA repair mechanisms which compromises genomic stability and favors a mutator phenotype. Among an increasing pool of mutated factors, regulators of DNA methylation are frequently found in t(8;21) AML. Together with the alteration of both, histone markers and distal enhancer regulation, RUNX1-ETO might specifically disrupt normal chromatin structure. Epigenetic studies on the fusion protein uncovered new mechanisms contributing to leukemogenesis and hopefully will translate into clinical applications.</jats:p> RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia International Journal of Molecular Sciences |
| spellingShingle | van der Kouwe, Emiel, Staber, Philipp, International Journal of Molecular Sciences, RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia, Inorganic Chemistry, Organic Chemistry, Physical and Theoretical Chemistry, Computer Science Applications, Spectroscopy, Molecular Biology, General Medicine, Catalysis |
| title | RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia |
| title_full | RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia |
| title_fullStr | RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia |
| title_full_unstemmed | RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia |
| title_short | RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia |
| title_sort | runx1-eto: attacking the epigenome for genomic instable leukemia |
| title_unstemmed | RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia |
| topic | Inorganic Chemistry, Organic Chemistry, Physical and Theoretical Chemistry, Computer Science Applications, Spectroscopy, Molecular Biology, General Medicine, Catalysis |
| url | http://dx.doi.org/10.3390/ijms20020350 |