ArticleNature communications2022
HOXA9 has the hallmarks of a biological switch with implications in blood cancers.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Tet2 deficiency drives age-related heterogeneous progression of myeloid neoplasms through epigenetic-immune microenvironment imbalance.Journal of translational medicine · 2026Article
- IMOP-Cancer: identifying mutation order pairs impacting cancer phenotypes.Briefings in bioinformatics · 2025Article
- Hypermethylation ofCurrent issues in molecular biology · 2025Article
- Potential role of miR-29b from mesenchymal stromal cell-derived extracellular vesicles in leukemic cell progression.PloS one · 2025Article
- HOXA9 transcription factor is a double-edged sword: from development to cancer progression.Cancer metastasis reviews · 2024Review
- Order-of-Mutation Effects on Cancer Progression: Models for Myeloproliferative Neoplasm.Bulletin of mathematical biology · 2024Article
- Exploring the expression and clinical significance of the miR-140-3p-HOXA9 axis in colorectal cancer.Journal of cancer research and clinical oncology · 2024Article
- HOXA9 Regulome and Pharmacological Interventions in Leukemia.Advances in experimental medicine and biology · 2024Review
- Review
- HOXA9 has the hallmarks of a biological switch with implications in blood cancers.Nature communications · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Blood malignancies arise from the dysregulation of haematopoiesis. The type of blood cell and the specific order of oncogenic events initiating abnormal growth ultimately determine the cancer subtype and subsequent clinical outcome. HOXA9 plays an important role in acute myeloid leukaemia (AML) prognosis by promoting blood cell expansion and altering differentiation; however, the function of HOXA9 in other blood malignancies is still unclear. Here, we highlight the biological switch and prognosis marker properties of HOXA9 in AML and chronic myeloproliferative neoplasms (MPN). First, we establish the ability of HOXA9 to stratify AML patients with distinct cellular and clinical outcomes. Then, through the use of a computational network model of MPN, we show that the self-activation of HOXA9 and its relationship to JAK2 and TET2 can explain the branching progression of JAK2/TET2 mutant MPN patients towards divergent clinical characteristics. Finally, we predict a connection between the RUNX1 and MYB genes and a suppressive role for the NOTCH pathway in MPN diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.