ReviewJournal of hematology & oncology2014
Targeting hedgehog signaling in myelofibrosis and other hematologic malignancies.
Review in Journal of hematology & oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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
26 citing papers in PubMed, 39 citations in OpenAlex.
- Safety and efficacy of the combination of sonidegib and ruxolitinib in myelofibrosis: a phase 1b/2 dose-finding study.Blood advances · 2020Trial
- Oncogenic activation of EVC/EVC2 defines a therapeutically targetable subset of acute myeloid leukemia.Leukemia · 2026Article
- Hedgehog Signaling Pathway in Fibrosis and Targeted Therapies.Biomolecules · 2024Review
- The Role of Mutated Calreticulin in the Pathogenesis ofInternational journal of molecular sciences · 2024Article
- Shh Gene Regulates the Proliferation and Apoptosis of Dermal Papilla Cells to Affect Its Differential Expression in Secondary Hair Follicle Growth Cycle of Cashmere Goats.Animals : an open access journal from MDPI · 2024Article
- Phase 1/1b study of azacitidine and hedgehog pathway inhibitor sonidegib in patients with myeloid neoplasms.Cancer · 2023Article
- Systematic dissection of coordinated stromal remodeling identifies Sox10Cell stem cell · 2023Article
- Transcriptomic Analysis Reveals JAK2/MPL-Independent Effects of Calreticulin Mutations in aCells · 2023Article
- Profile of Glasdegib for the Treatment of Newly Diagnosed Acute Myeloid Leukemia (AML): Evidence to Date.Cancer management and research · 2022Review
- Finding a Jill for JAK: Assessing Past, Present, and Future JAK Inhibitor Combination Approaches in Myelofibrosis.Cancers · 2020Review
- Bone marrow niche dysregulation in myeloproliferative neoplasms.Haematologica · 2020Review
- Beyond Ruxolitinib: Fedratinib and Other Emergent Treatment Options for Myelofibrosis.Cancer management and research · 2019Review
- A phase Ib study to assess the efficacy and safety of vismodegib in combination with ruxolitinib in patients with intermediate- or high-risk myelofibrosis.Journal of hematology & oncology · 2018Article
- Hedgehog Signaling: From Basic Biology to Cancer Therapy.Cell chemical biology · 2017Review
- Bone marrow fibrosis in myelofibrosis: pathogenesis, prognosis and targeted strategies.Haematologica · 2016Review
- Second- and third-generation ALK inhibitors for non-small cell lung cancer.Journal of hematology & oncology · 2016Review
- New Strategies in Myeloproliferative Neoplasms: The Evolving Genetic and Therapeutic Landscape.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Review
- Bone marrow fibrosis in primary myelofibrosis: pathogenic mechanisms and the role of TGF-β.Stem cell investigation · 2016Review
- Novel agents for advanced pancreatic cancer.Oncotarget · 2015Review
- The Hedgehog pathway as targetable vulnerability with 5-azacytidine in myelodysplastic syndrome and acute myeloid leukemia.Journal of hematology & oncology · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Treatment of myelofibrosis (MF), a BCR-ABL-negative myeloproliferative neoplasm, is challenging. The only current potentially curative option, allogeneic hematopoietic stem cell transplant, is recommended for few patients. The remaining patients are treated with palliative therapies to manage MF-related anemia and splenomegaly. Identification of a mutation in the Janus kinase 2 (JAK2) gene (JAK2 V617F) in more than half of all patients with MF has prompted the discovery and clinical development of inhibitors that target JAK2. Although treatment with JAK2 inhibitors has been shown to improve symptom response and quality of life in patients with MF, these drugs do not alter the underlying disease; therefore, novel therapies are needed. The hedgehog (Hh) signaling pathway has been shown to play a role in normal hematopoiesis and in the tumorigenesis of hematologic malignancies. Moreover, inhibitors of the Hh pathway have been shown to inhibit growth and self-renewal capacity in preclinical models of MF. In a mouse model of MF, combined inhibition of the Hh and JAK pathways reduced JAK2 mutant allele burden, reduced bone marrow fibrosis, and reduced white blood cell and platelet counts. Preliminary clinical data also suggest that inhibition of the Hh pathway, alone or in combination with JAK2 inhibition, may enable disease modification in patients with MF. Future studies, including one combining the Hh pathway inhibitor sonidegib and the JAK2 inhibitor ruxolitinib, are underway in patients with MF and will inform whether this combination approach can lead to true disease modification.
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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.