ArticlePloS one2015
JAK2V617F drives Mcl-1 expression and sensitizes hematologic cell lines to dual inhibition of JAK2 and Bcl-xL.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Preliminary Safety and Efficacy of Navitoclax Plus Ruxolitinib in Janus Kinase Inhibitor-Naïve Patients With Myelofibrosis From the Multicenter, Open-Label, Phase 2 Study (REFINE).Hematological oncology · 2026Trial
- Addition of navitoclax to ruxolitinib for patients with myelofibrosis with progression or suboptimal response.Blood neoplasia · 2025Trial
- Addition of Navitoclax to Ongoing Ruxolitinib Therapy for Patients With Myelofibrosis With Progression or Suboptimal Response: Phase II Safety and Efficacy.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2022Trial
- Semi-Mechanistic PK/PD Modeling of Platelets and Spleen Volume With Navitoclax in Combination With Ruxolitinib in Patients With Myelofibrosis.CPT: pharmacometrics & systems pharmacology · 2026Article
- Targeting BCL-xL in Myeloid Malignancies: From Inhibitors to PROTAC.Journal of cellular and molecular medicine · 2026Review
- Malignant JAK-signaling: at the interface of inflammation and malignant transformation.Leukemia · 2025Review
- Pharmacokinetics and Safety of Navitoclax in Hepatic Impairment.Clinical pharmacokinetics · 2025Article
- The survivin/XIAP suppressant YM155 impairs clonal growth and induces apoptosis in JAK2Hematology, transfusion and cell therapy · 2024Article
- Targeted Therapy for MPNs: Going Beyond JAK Inhibitors.Current hematologic malignancy reports · 2023Review
- Review
- Article
- Putative Role of Neutrophil Extracellular Trap Formation in Chronic Myeloproliferative Neoplasms.International journal of molecular sciences · 2023Review
- Treating accelerated and blast phase myeloproliferative neoplasms: progress and challenges.Therapeutic advances in hematology · 2023Review
- Acute Myeloid Leukemia Following Myeloproliferative Neoplasms: A Review of What We Know, What We Do Not Know, and Emerging Treatment Strategies.Journal of hematology · 2022Review
- Apoptosis: Directly Targeted at Last.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2022Article
- Neutrophil Death in Myeloproliferative Neoplasms: Shedding More Light on Neutrophils as a Pathogenic Link to Chronic Inflammation.International journal of molecular sciences · 2022Review
- Article
- Finding a Jill for JAK: Assessing Past, Present, and Future JAK Inhibitor Combination Approaches in Myelofibrosis.Cancers · 2020Review
- Autophagy inhibition potentiates ruxolitinib-induced apoptosis in JAK2Investigational new drugs · 2020Article
- Reversine exhibits antineoplastic activity in JAK2Scientific reports · 2019Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Constitutive activation of the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) axis is fundamental to the molecular pathogenesis of a host of hematological disorders, including acute leukemias and myeloproliferative neoplasms (MPN). We demonstrate here that the major JAK2 mutation observed in these diseases (JAK2V617F) enforces Mcl-1 transcription via STAT3 signaling. Targeting this lesion with JAK inhibitor I (JAKi-I) attenuates STAT3 binding to the Mcl-1 promoter and suppresses Mcl-1 transcript and protein expression. The neutralization of Mcl-1 in JAK2V617F-harboring myelodyssplastic syndrome cell lines sensitizes them to apoptosis induced by the BH3-mimetic and Bcl-xL/Bcl-2 inhibitor, ABT-263. Moreover, simultaneously targeting JAK and Bcl-xL/-2 is synergistic in the presence of the JAK2V617F mutation. These findings suggest that JAK/Bcl-xL/-2 inhibitor combination therapy may have applicability in a range of hematological disorders characterized by activating JAK2 mutations.
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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.