ArticleNature communications2023
Proteogenetic drug response profiling elucidates targetable vulnerabilities of myelofibrosis.
Article in Nature communications, 2023. 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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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- A tumor profiling resource for ovarian cancer: insights into chemotherapy-driven heterogeneity and personalized treatment strategy.Nature communications · 2026Article
- Immunogenetic and Transcriptomic Evidence Implicating the NKG2D-MICA/MICB Axis in CALR-Mutated Myeloproliferative Neoplasms.Cancers · 2026Article
- A tissue-specific atlas of protein-protein associations enables prioritization of candidate disease genes.Nature biotechnology · 2026Article
- Review
- Identification of candidate proteins influencing spermatogenesis in Shandong black cattle via integrated multiomics analysis.BMC genomics · 2025Article
- MultiOmicsAgent: Guided Extreme Gradient-Boosted Decision Trees-Based Approaches for Biomarker-Candidate Discovery in Multiomics Data.Journal of proteome research · 2025Article
- Malignant JAK-signaling: at the interface of inflammation and malignant transformation.Leukemia · 2025Review
- Paediatric Personalized Research Network Switzerland (SwissPedHealth): a joint paediatric national data stream.BMJ open · 2024Article
- Star wars against leukemia: attacking the clones.Leukemia · 2024Review
- Single-cell landscape of innate and acquired drug resistance in acute myeloid leukemia.Nature communications · 2024Article
- Applications of artificial intelligence to myeloproliferative neoplasms: a narrative review.Expert review of hematology · 2024Review
- Molecular Genetic Profile of Myelofibrosis: Implications in the Diagnosis, Prognosis, and Treatment Advancements.Cancers · 2024Review
Corrections and comments
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Authors and funding
21 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myelofibrosis is a hematopoietic stem cell disorder belonging to the myeloproliferative neoplasms. Myelofibrosis patients frequently carry driver mutations in either JAK2 or Calreticulin (CALR) and have limited therapeutic options. Here, we integrate ex vivo drug response and proteotype analyses across myelofibrosis patient cohorts to discover targetable vulnerabilities and associated therapeutic strategies. Drug sensitivities of mutated and progenitor cells were measured in patient blood using high-content imaging and single-cell deep learning-based analyses. Integration with matched molecular profiling revealed three targetable vulnerabilities. First, CALR mutations drive BET and HDAC inhibitor sensitivity, particularly in the absence of high Ras pathway protein levels. Second, an MCM complex-high proliferative signature corresponds to advanced disease and sensitivity to drugs targeting pro-survival signaling and DNA replication. Third, homozygous CALR mutations result in high endoplasmic reticulum (ER) stress, responding to ER stressors and unfolded protein response inhibition. Overall, our integrated analyses provide a molecularly motivated roadmap for individualized myelofibrosis patient treatment.
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