RUNX1/ETO and mutant KIT both contribute to programming the transcriptional and chromatin landscape in t(8;21) acute myeloid leukemia

Chin, Paulynn Suyin; Assi, Salam A.; Ptasińska, Anetta; Imperato, Maria Rosaria; Cockerill, Peter N.; Bonifer, Constanze

doi:10.1016/j.exphem.2020.10.005

Cited by 2 publications

(1 citation statement)

References 37 publications

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“…In line with these observations, Chin and colleagues confirmed the oncogenic cooperation of RUNX1::RUNX1T1 with c-KIT(N822K) in human cord blood CD34+ cells. In their model, RUNX1::RUNX1T1 + c-KIT(N822K) also displayed growth advantage, enhanced expansion ability, and clonogenic potential compared to RUNX1::RUNX1T1 alone [ 91 ]. As mentioned, RUNX1::RUNX1T1 alone was not able to induce leukemogenesis in mice, prompting the question of additional co-activators necessary to induce leukemia in mice [ 92 ].…”

Section: “Two-hit” Models For Human Cd34+ Ex Vivo Progenitor Cell Exp...mentioning

confidence: 99%

Deciphering Acute Myeloid Leukemia Associated Transcription Factors in Human Primary CD34+ Hematopoietic Stem/Progenitor Cells

Kreissig,

Windisch,

Wichmann

2023

Cells

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Hemato-oncological diseases account for nearly 10% of all malignancies and can be classified into leukemia, lymphoma, myeloproliferative diseases, and myelodysplastic syndromes. The causes and prognosis of these disease entities are highly variable. Most entities are not permanently controllable and ultimately lead to the patient’s death. At the molecular level, recurrent mutations including chromosomal translocations initiate the transformation from normal stem-/progenitor cells into malignant blasts finally floating the patient’s bone marrow and blood system. In acute myeloid leukemia (AML), the so-called master transcription factors such as RUNX1, KMT2A, and HOX are frequently disrupted by chromosomal translocations, resulting in neomorphic oncogenic fusion genes. Triggering ex vivo expansion of primary human CD34+ stem/progenitor cells represents a distinct characteristic of such chimeric AML transcription factors. Regarding oncogenic mechanisms of AML, most studies focus on murine models. However, due to biological differences between mice and humans, findings are only partly transferable. This review focuses on the genetic manipulation of human CD34+ primary hematopoietic stem/progenitor cells derived from healthy donors to model acute myeloid leukemia cell growth. Analysis of defined single- or multi-hit human cellular AML models will elucidate molecular mechanisms of the development, maintenance, and potential molecular intervention strategies to counteract malignant human AML blast cell growth.

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Section: “Two-hit” Models For Human Cd34+ Ex Vivo Progenitor Cell Exp...mentioning

confidence: 99%

Deciphering Acute Myeloid Leukemia Associated Transcription Factors in Human Primary CD34+ Hematopoietic Stem/Progenitor Cells

Kreissig,

Windisch,

Wichmann

2023

Cells

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The Prognostic Significance of c-KIT Mutations in Core Binding Factor Acute Myeloid Leukemia

Shafik

Ibraheem

Selim

et al. 2022

Clinical Lymphoma Myeloma and Leukemia

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RUNX1/ETO and mutant KIT both contribute to programming the transcriptional and chromatin landscape in t(8;21) acute myeloid leukemia

Cited by 2 publications

References 37 publications

Deciphering Acute Myeloid Leukemia Associated Transcription Factors in Human Primary CD34+ Hematopoietic Stem/Progenitor Cells

Deciphering Acute Myeloid Leukemia Associated Transcription Factors in Human Primary CD34+ Hematopoietic Stem/Progenitor Cells

The Prognostic Significance of c-KIT Mutations in Core Binding Factor Acute Myeloid Leukemia

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