ArticleBlood advances2022
HMGA2 expression defines a subset of human AML with immature transcriptional signature and vulnerability to G2/M inhibition.
Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 17 citations in OpenAlex.
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- IL1RAP is an immunotherapeutic target for normal karyotype triple-mutated acute myeloid leukemia.Biomarker research · 2025Article
- HMGA2 overexpression with specific chromosomal abnormalities predominate in CALR and ASXL1 mutated myelofibrosis.Leukemia · 2025Article
- High Mobility Group A1 Chromatin Keys: Unlocking the Genome During MPN Progression.International journal of molecular sciences · 2025Review
- Auto-expansion ofMolecular therapy. Methods & clinical development · 2024Article
- Chromatin modifier Hmga2 promotes adult hematopoietic stem cell function and blood regeneration in stress conditions.The EMBO journal · 2024Article
- HMGA2 promotes platelet-neutrophil complex formation and pulmonary tissue damage in myelodysplastic syndromes.Blood vessels, thrombosis & hemostasis · 2024Article
- Article
- Cellular carcinogenesis in preleukemic conditions:drivers and defenses.Fukushima journal of medical science · 2024Review
- Aberrant stem cell and developmental programs in pediatric leukemia.Frontiers in cell and developmental biology · 2024Review
- Single-cell transcriptomics identifies adipose tissue CD271Cell reports. Medicine · 2023Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-mobility group AT-hook 2 (HMGA2) is a nonhistone chromatin-binding protein that is normally expressed in stem cells of various tissues and aberrantly detected in several tumor types. We recently observed that one-fourth of human acute myeloid leukemia (AML) specimens express HMGA2, which associates with a very poor prognosis. We present results indicating that HMGA2+ AMLs share a distinct transcriptional signature representing an immature phenotype. Using single-cell analyses, we showed that HMGA2 is expressed in CD34+ subsets of stem cells and early progenitors, whether normal or derived from AML specimens. Of interest, we found that one of the strongest gene expression signatures associated with HMGA2 in AML is the upregulation of G2/M checkpoint genes. Whole-genome CRISPR/Cas9 screening in HMGA2 overexpressing cells further revealed a synthetic lethal interaction with several G2/M checkpoint genes. Accordingly, small molecules that target G2/M proteins were preferentially active in vitro and in vivo on HMGA2+ AML specimens. Together, our findings suggest that HMGA2 is a key functional determinant in AML and is associated with stem cell features, G2/M status, and related drug sensitivity.
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