ReviewMolecular cancer2018
Targeting few to help hundreds: JAK, MAPK and ROCK pathways as druggable targets in atypical chronic myeloid leukemia.
Review in Molecular cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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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
21 citing papers in PubMed, 30 citations in OpenAlex.
- Efficacy of Ruxolitinib in Patients With Chronic Neutrophilic Leukemia and Atypical Chronic Myeloid Leukemia.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2020Trial
- Liver diseases: epidemiology, causes, trends and predictions.Signal transduction and targeted therapy · 2025Review
- LDLRAD4 is a potential diagnostic and prognostic biomarker correlated with immune infiltration in myelodysplastic syndromes.Frontiers in genetics · 2025Article
- Comprehensive analysis of Atypical chronic myeloid leukemia (aCML): Epidemiology, clinical features, and survival outcomes based on SEER database insights.Leukemia research reports · 2025Article
- Atypical chronic myeloid leukemia found in a patient with eosinophilia for six years: a case report.BMC geriatrics · 2024Article
- miR-15a targets the HSP90 co-chaperone Morgana in chronic myeloid leukemia.Scientific reports · 2024Article
- JAK/STAT blockade reverses the malignant phenotype of Hodgkin and Reed-Sternberg cells.Blood advances · 2023Article
- CNL and aCML should be considered as a single entity based on molecular profiles and outcomes.Blood advances · 2023Article
- Article
- Understanding Aberrant Signaling to Elude Therapy Escape Mechanisms in Myeloproliferative Neoplasms.Cancers · 2022Review
- Bioluminescent Zebrafish Transplantation Model for Drug Discovery.Frontiers in pharmacology · 2022Article
- The Hippo signaling pathway in leukemia: function, interaction, and carcinogenesis.Cancer cell international · 2021Review
- MiR-125a-3p and MiR-320b Differentially Expressed in Patients with Chronic Myeloid Leukemia Treated with Allogeneic Hematopoietic Stem Cell Transplantation and Imatinib Mesylate.International journal of molecular sciences · 2021Article
- Article
- Molecular pathogenesis of the myeloproliferative neoplasms.Journal of hematology & oncology · 2021Review
- KD025, an anti-adipocyte differentiation drug, enhances the efficacy of conventional chemotherapeutic drugs in ABCG2-overexpressing leukemia cells.Oncology letters · 2020Article
- Atypical Chronic Myeloid Leukemia: Where Are We Now?International journal of molecular sciences · 2020Review
- Systematic Analysis of Autophagy-Related Signature Uncovers Prognostic Predictor for Acute Myeloid Leukemia.DNA and cell biology · 2020Article
- Next-generation sequencing reveals unique combination of mutations in cis of CSF3R in atypical chronic myeloid leukemia.Journal of clinical laboratory analysis · 2020Article
- Comparison of microRNA Expression Profile in Chronic Myeloid Leukemia Patients Newly Diagnosed and Treated by Allogeneic Hematopoietic Stem Cell Transplantation.Frontiers in oncology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Atypical Chronic Myeloid Leukemia (aCML) is a myeloproliferative neoplasm characterized by neutrophilic leukocytosis and dysgranulopoiesis. From a genetic point of view, aCML shows a heterogeneous mutational landscape with mutations affecting signal transduction proteins but also broad genetic modifiers and chromatin remodelers, making difficult to understand the molecular mechanisms causing the onset of the disease. The JAK-STAT, MAPK and ROCK pathways are known to be responsible for myeloproliferation in physiological conditions and to be aberrantly activated in myeloproliferative diseases. Furthermore, experimental evidences suggest the efficacy of inhibitors targeting these pathways in repressing myeloproliferation, opening the way to deep clinical investigations. However, the activation status of these pathways is rarely analyzed when genetic mutations do not occur in a component of the signaling cascade. Given that mutations in functionally unrelated genes give rise to the same pathology, it is tempting to speculate that alteration in the few signaling pathways mentioned above might be a common feature of pathological myeloproliferation. If so, targeted therapy would be an option to be considered for aCML patients.
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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.