ReviewMolecular diversity2024
JAK2 inhibitors for the treatment of Philadelphia-negative myeloproliferative neoplasms: current status and future directions.
Review in Molecular diversity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- Cucurbitacin derivatives (B, IIa, IIb, and E): modulating gut dysbiosis and inflammatory pathways for multi-target therapy of ulcerative colitis.Inflammopharmacology · 2026Review
- PD-1/PD-L1-CXCR3 Coexpression and CXCR3 on Intermediate Monocytes Predict Fibrosis, Leukemic Transformation, and Survival in Egyptian Philadelphia-Negative Myeloproliferative Neoplasms.Clinical Medicine Insights. Oncology · 2026Article
- DARS expression in BCR/ABL1-negative myeloproliferative neoplasms and its association with the immune microenvironment.Scientific reports · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The overactivation of Janus kinases 2 (JAK2) by gain-of-function mutations in the JAK2, Myeloproliferative leukemia virus oncogene, or Calreticulin genes are the most important factor in the development of Philadelphia-negative myeloproliferative neoplasms (MPNs). The discovery of the JAK2V617F mutation is a significant breakthrough in understanding the pathogenesis of MPNs, and inhibition of JAK2 abnormal activation has become one of the most effective strategies against MPNs. Currently, three JAK2 inhibitors for treating MPNs have been approved, and several are being evaluated in clinical trials. However, persistent challenges in terms of drug resistance and off-target effects remain unresolved. In this review, we introduce and classify the available JAK2 inhibitors in terms of their mechanisms and clinical considerations. Additionally, through an analysis of target points, binding modes, and structure-activity inhibitor relationships, we propose strategies such as combination therapy and allosteric inhibitors to overcome specific challenges. This review offers valuable insights into current trends and future directions for optimal management of MPNs using JAK2 inhibitors.
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Identifiers
What OpenQuestion holds
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.