ReviewOncogene2013
JAK/STAT signaling in hematological malignancies.
Review in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05063110 (Treatment of Non Severe Hemophagocytosis Lymphohistiocytosis With ITACITINIB a Phase II Prospective Trial), which is not on this map. Cited by 291 papers, 1 of them a synthesis that pooled it.
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.
Treatment of Non Severe Hemophagocytosis Lymphohistiocytosis With ITACITINIB a Phase II Prospective Trial
Who cites it
291 citing papers in PubMed, 1 synthesis or guideline pooled it, 532 citations in OpenAlex.
- The role of chemokines and interleukins in acute lymphoblastic leukemia: a systematic review.Journal of applied biomedicine · 2024Pooled it
- Trial
- Safety and efficacy of fedratinib, a selective oral inhibitor of Janus kinase-2 (JAK2), in patients with myelofibrosis and low pretreatment platelet counts.British journal of haematology · 2022Trial
- Ruxolitinib shows activity against Hodgkin lymphoma but not primary mediastinal large B-cell lymphoma.BMC cancer · 2019Trial
- Population pharmacokinetics of fedratinib in patients with myelofibrosis, polycythemia vera, and essential thrombocythemia.Cancer chemotherapy and pharmacology · 2019Trial
- Association between JAK2 mutations and thoracic aortic aneurysms in myeloproliferative neoplasms.Journal of thrombosis and thrombolysis · 2026Review
- Greatwall kinase regulates acute myeloid leukaemia cell division through a non-canonical mechanism.EMBO reports · 2026Article
- Identifying JAK2 and ANXA5 as Key Genes Linking Obstructive Sleep Apnea and Oxidative Stress via Machine Learning and Multilayer Transcriptomic Integration With Functional Validation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Multi-Omics Characterization of Peripheral Blood Molecular Profiles in Hypertensive AgingAnimals : an open access journal from MDPI · 2026Article
- Upadacitinib enhances platelet procoagulant responses in a subset of healthy individuals and patients with SLE: a pilot study.Lupus science & medicine · 2026Article
- Computational design of synthetic receptors with programmable signalling activity for enhanced cancer T cell therapy.Nature biomedical engineering · 2026Article
- SETD2 inhibited T-cell acute lymphocytic leukemia invasion and infiltration by inhibiting the JAK/STAT pathway.Molecular and cellular biochemistry · 2026Article
- The antitumor mechanism of oclacitinib in canine lymphoma.Scientific reports · 2026Article
- JAK inhibition in PD-1 immunotherapy and tumor microenvironment.Frontiers in immunology · 2026Review
- STAT3 SH2 Domain Aspartic Acid 661 Mutations Activate Immune Gene Programs.Journal of cellular and molecular medicine · 2026Article
- Genetic and chromosomal dysregulations of progenitor cells in the etiology and pathogenesis of pediatric cancers.American journal of stem cells · 2026Review
- In silico modeling guides identification of novel JAK1 variants associated with immune dysregulation.EMBO molecular medicine · 2025Article
- Deciphering and targeting oncogenic pathways through integrated approaches and amino acid metabolism in hematologic malignancies.Discover oncology · 2025Review
- STAT1-mediated epigenetic regulation of LIN28A controls iPSC-derived platelet production through the let-7-RALB axis.Blood advances · 2025Article
- Polydatin: A natural compound with multifaceted anticancer properties.Journal of traditional and complementary medicine · 2025Review
231 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway is central to signaling by cytokine receptors, a superfamily of more than 30 transmembrane proteins that recognize specific cytokines, and is critical in blood formation and immune response. Many of those receptors transmit anti-apoptotic, proliferative and differentiation signals, and their expression and functions are critical for the formation of blood lineages. Several cancers, including blood malignancies, have been associated with constitutive activation of members of the STAT family, which normally require JAK-mediated tyrosine phosphorylation for transcriptional activation. More recently, human myeloproliferative neoplasms were discovered to be associated with a unique acquired somatic mutation in JAK2 (JAK2 V617F), rare exon 12 JAK2 mutations, or thrombopoietin receptor mutations that constitutively activate wild-type JAK2. Prompted by these observations, many studies have explored the possibility that JAKs, cytokine receptors, or other components of the JAK/STAT pathway are mutated or upregulated in several hematological malignancies. This has been observed in certain pediatric acute lymphoblastic leukemias and adult T-cell lymphoblastic leukemias, and overexpression of JAK2 seems to be important in Hodgkin lymphoma. Here we discuss the nature and respective contribution of mutations dysregulating the JAK/STAT pathway in hematological malignancies and present examples in which such mutations drive the disease, contribute to the phenotype, or provide a survival and proliferative advantage. JAK inhibitors are making their way into the therapeutic arsenal (for example, in myelofibrosis), and we discuss the possibility that other hematological diseases might benefit from treatment with these inhibitors in combination with other agents.
Indexed as
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.