ReviewHaematologica2015
JAK kinase targeting in hematologic malignancies: a sinuous pathway from identification of genetic alterations towards clinical indications.
Review in Haematologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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
32 citing papers in PubMed, 61 citations in OpenAlex.
- Synergistic cooperation between progranulin and Jak2/Stat3 signaling determines definitive myeloid cell fate.Cell reports · 2026Article
- Insights into IL-6/JAK/STAT3 signaling in the tumor microenvironment: Implications for cancer therapy.Cytokine & growth factor reviews · 2025Review
- The Mechanisms of Resistance to JAK Inhibitors in Lymphoid Leukemias: A Scoping Review of Evidence from Preclinical Models and Case Reports.International journal of molecular sciences · 2025Article
- Comprehensive Safety Exposure-Response Analysis to Support Ritlecitinib Dose Selection.CPT: pharmacometrics & systems pharmacology · 2025Article
- Direct STAT3 and STAT5 Inhibition Overcomes Treatment Resistance in a Murine-Derived in vitro Model of Acute Lymphoblastic Leukaemia Driven by <italic>ETV6::JAK2</italic>.Acta haematologica · 2025Article
- The oncogenic mechanisms of the Janus kinase-signal transducer and activator of transcription pathway in digestive tract tumors.Cell communication and signaling : CCS · 2024Review
- JAK2 as Predictor of Therapeutic Response in Patients with Chronic Myeloid Leukemia Treated with Imatinib.Disease markers · 2024Article
- Article
- Direct and indirect effects of IFN-α2b in malignancy treatment: not only an archer but also an arrow.Biomarker research · 2022Review
- Ruxolitinib Reduces Oxidative Stress in Patients With Primary Myelofibrosis: A Multicenter Study.Cureus · 2022Article
- Extracellular matrix protein N-glycosylation mediates immune self-tolerance inProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Acquired JAK2 mutations confer resistance to JAK inhibitors in cell models of acute lymphoblastic leukemia.NPJ precision oncology · 2021Article
- Expression of RUNX1-JAK2 in Human Induced Pluripotent Stem Cell-Derived Hematopoietic Cells Activates the JAK-STAT and MYC Pathways.International journal of molecular sciences · 2021Article
- Investigation of a new oxazolidine derivative in human resistance acute leukemia cells: deciphering its mechanism of action by label-free proteomic.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Review
- JAK-STAT in Early Hematopoiesis and Leukemia.Frontiers in cell and developmental biology · 2021Review
- Inflammation-driven activation of JAK/STAT signaling reversibly accelerates acute myeloid leukemia in vitro.Blood advances · 2020Article
- Multi-parametric single cell evaluation defines distinct drug responses in healthy hematologic cells that are retained in corresponding malignant cell types.Haematologica · 2020Article
- Drug-Related Cutaneous Adverse Events in Philadelphia Chromosome-Negative Myeloproliferative Neoplasms: A Literature Review.International journal of molecular sciences · 2020Review
- Cytokine receptor splice variants in hematologic diseases.Cytokine · 2020Review
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Constitutive JAK-STAT pathway activation occurs in most myeloproliferative neoplasms as well as in a significant proportion of other hematologic malignancies, and is frequently a marker of poor prognosis. The underlying molecular alterations are heterogeneous as they include activating mutations in distinct components (cytokine receptor, JAK, STAT), overexpression (cytokine receptor, JAK) or rare JAK2 fusion proteins. In some cases, concomitant loss of negative regulators contributes to pathogenesis by further boosting the activation of the cascade. Exploiting the signaling bottleneck provided by the limited number of JAK kinases is an attractive therapeutic strategy for hematologic neoplasms driven by constitutive JAK-STAT pathway activation. However, given the conserved nature of the kinase domain among family members and the interrelated roles of JAK kinases in many physiological processes, including hematopoiesis and immunity, broad usage of JAK inhibitors in hematology is challenged by their narrow therapeutic window. Novel therapies are, therefore, needed. The development of more selective inhibitors is a questionable strategy as such inhibitors might abrogate the beneficial contribution of alleviating the cancer-related pro-inflammatory microenvironment and raise selective pressure to a threshold that allows the emergence of malignant subclones harboring drug-resistant mutations. In contrast, synergistic combinations of JAK inhibitors with drugs targeting cascades that work in concert with JAK-STAT pathway appear to be promising therapeutic alternatives to JAK inhibitors as monotherapies.
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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.