ArticleBlood2022
BMP2/SMAD pathway activation in JAK2/p53-mutant megakaryocyte/erythroid progenitors promotes leukemic transformation.
Article in Blood, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Acute myeloid leukemia with bipotential erythroid and megakaryocytic differentiation: a case series and literature review.Journal of hematopathology · 2025Pooled it
- Defining and predicting disease progression in myeloproliferative neoplasms: a proposed biomarker-driven approach.Leukemia · 2026Review
- Single-cell long-read genotyping of transcripts reveals discrete mechanisms of clonal evolution in post-MPN AML.Blood advances · 2026Article
- Genomic insights transform diagnosis, prognosis, and therapy in BCR::ABL1-negative myeloproliferative neoplasms.International journal of hematology · 2026Review
- Distinct stem cell identities converge into shared erythroid stress in ERCC6L2 disease and Shwachman-Diamond syndrome.HemaSphere · 2026Article
- Epidemiology and prognostic factors of acute erythroid leukemia.Translational cancer research · 2026Article
- JAK2V617F reprograms Hypoxia Inducible Factor-1 to induce a non-canonical hypoxia regulon in myeloproliferative neoplasms.Leukemia · 2026Article
- Unraveling the role ofHemaSphere · 2026Review
- C-C motif chemokine receptor-like 2 promotes the interferon-γ signaling response in myeloid neoplasms with erythroid differentiation and mutatedHaematologica · 2026Article
- BCL-XL drives fibrotic and leukemic progression in myeloproliferative neoplasms.Frontiers in immunology · 2026Article
- SIRT5-mediated regulation of BMP2 succinylation enhances osteogenic differentiation of BMSCs and promotes tibial fracture healing.Stem cell research & therapy · 2025Article
- Preclinical efficacy of tasquinimod-based combinations in advanced myeloproliferative neoplasms in blastic phase.Blood advances · 2025Article
- MiR-218 Exhibits Anti-Leukemia Effects by Targeting CTNND2 in Primary Acute Erythroid Leukemia HEL Cells.Cell biochemistry and biophysics · 2025Article
- Transcriptomic Signatures in TP53 Positive and Negative Tumor Samples in NSCLC.Current gene therapy · 2025Article
- Efficacy of a novel BCL-xL degrader, DT2216, in preclinical models of JAK2-mutated post-MPN AML.Blood · 2025Article
- A correlation of ineffective erythropoiesis and dysregulated signaling pathways in myelodysplastic syndromes/neoplasms.Experimental hematology & oncology · 2025Article
- Pathogenesis and management of high molecular risk myeloproliferative neoplasms.Haematologica · 2025Review
- Prevention and treatment of transformation of myeloproliferative neoplasms to acute myeloid leukemia.Haematologica · 2025Review
- Versatility of megakaryocytes in homeostasis and disease.Blood science (Baltimore, Md.) · 2024Review
- Cinnamaldehyde Regulates the Migration and Apoptosis of Gastric Cancer Cells by Inhibiting the Jak2/Stat3 Pathway.Digestive diseases and sciences · 2024Article
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Authors and funding
18 authors at 6 institutions in 2 countries.
Funding
Abstract
Leukemic transformation (LT) of myeloproliferative neoplasm (MPN) has a dismal prognosis and is largely fatal. Mutational inactivation of TP53 is the most common somatic event in LT; however, the mechanisms by which TP53 mutations promote LT remain unresolved. Using an allelic series of mouse models of Jak2/Trp53 mutant MPN, we identify that only biallelic inactivation of Trp53 results in LT (to a pure erythroleukemia [PEL]). This PEL arises from the megakaryocyte-erythroid progenitor population. Importantly, the bone morphogenetic protein 2/SMAD pathway is aberrantly activated during LT and results in abnormal self-renewal of megakaryocyte-erythroid progenitors. Finally, we identify that Jak2/Trp53 mutant PEL is characterized by recurrent copy number alterations and DNA damage. Using a synthetic lethality strategy, by targeting active DNA repair pathways, we show that this PEL is highly sensitive to combination WEE1 and poly(ADP-ribose) polymerase inhibition. These observations yield new mechanistic insights into the process of p53 mutant LT and offer new, clinically translatable therapeutic approaches.
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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.