RUNX1 isoform disequilibrium promotes the development of trisomy 21–associated myeloid leukemia Article Swipe
S Gialesaki
,
Daniela Bräuer-Hartmann
,
H Issa
,
R Bhayadia
,
Oriol Alejo-Valle
,
Lonneke Verboon
,
A L Schmell
,
Stephanie Laszig
,
Enikő Regényi
,
K Schuschel
,
Maurice Labuhn
,
Michelle Ng
,
Robert L. Winkler
,
Christian Ihling
,
Andrea Sinz
,
Markus Glaß
,
Stefan Hüttelmaier
,
Sören Matzk
,
Lena Schmid
,
Farina Josepha Strüwe
,
Sofie‐Katrin Kadel
,
Dirk Reinhardt
,
Marie‐Laure Yaspo
,
Dirk Heckl
,
Jan‐Henning Klusmann
·
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.1182/blood.2022017619
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.1182/blood.2022017619
Gain of chromosome 21 (Hsa21) is among the most frequent aneuploidies in leukemia. However, it remains unclear how partial or complete amplifications of Hsa21 promote leukemogenesis and why children with Down syndrome (DS) (ie, trisomy 21) are particularly at risk of leukemia development. Here, we propose that RUNX1 isoform disequilibrium with RUNX1A bias is key to DS-associated myeloid leukemia (ML-DS). Starting with Hsa21-focused CRISPR–CRISPR-associated protein 9 screens, we uncovered a strong and specific RUNX1 dependency in ML-DS cells. Expression of the RUNX1A isoform is elevated in patients with ML-DS, and mechanistic studies using murine ML-DS models and patient-derived xenografts revealed that excess RUNX1A synergizes with the pathognomonic Gata1s mutation during leukemogenesis by displacing RUNX1C from its endogenous binding sites and inducing oncogenic programs in complex with the MYC cofactor MAX. These effects were reversed by restoring the RUNX1A:RUNX1C equilibrium in patient-derived xenografts in vitro and in vivo. Moreover, pharmacological interference with MYC:MAX dimerization using MYCi361 exerted strong antileukemic effects. Thus, our study highlights the importance of alternative splicing in leukemogenesis, even on a background of aneuploidy, and paves the way for the development of specific and targeted therapies for ML-DS, as well as for other leukemias with Hsa21 aneuploidy or RUNX1 isoform disequilibrium.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1182/blood.2022017619
- https://ashpublications.org/blood/article-pdf/141/10/1105/2037408/blood_bld-2022-017619-main.pdf
- OA Status
- hybrid
- Cited By
- 36
- References
- 62
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4311025083
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4311025083Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1182/blood.2022017619Digital Object Identifier
- Title
-
RUNX1 isoform disequilibrium promotes the development of trisomy 21–associated myeloid leukemiaWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2022Year of publication
- Publication date
-
2022-12-09Full publication date if available
- Authors
-
S Gialesaki, Daniela Bräuer-Hartmann, H Issa, R Bhayadia, Oriol Alejo-Valle, Lonneke Verboon, A L Schmell, Stephanie Laszig, Enikő Regényi, K Schuschel, Maurice Labuhn, Michelle Ng, Robert L. Winkler, Christian Ihling, Andrea Sinz, Markus Glaß, Stefan Hüttelmaier, Sören Matzk, Lena Schmid, Farina Josepha Strüwe, Sofie‐Katrin Kadel, Dirk Reinhardt, Marie‐Laure Yaspo, Dirk Heckl, Jan‐Henning KlusmannList of authors in order
- Landing page
-
https://doi.org/10.1182/blood.2022017619Publisher landing page
- PDF URL
-
https://ashpublications.org/blood/article-pdf/141/10/1105/2037408/blood_bld-2022-017619-main.pdfDirect link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
hybridOpen access status per OpenAlex
- OA URL
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https://ashpublications.org/blood/article-pdf/141/10/1105/2037408/blood_bld-2022-017619-main.pdfDirect OA link when available
- Concepts
-
Biology, RUNX1, Trisomy, Myeloid leukemia, Leukemia, Cancer research, Gene isoform, Myeloid, Down syndrome, Genetics, Molecular biology, Haematopoiesis, Stem cell, GeneTop concepts (fields/topics) attached by OpenAlex
- Cited by
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36Total citation count in OpenAlex
- Citations by year (recent)
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2025: 14, 2024: 14, 2023: 8Per-year citation counts (last 5 years)
- References (count)
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62Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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