ReviewFrontiers in oncology2025
Advances in the role of the IGF signaling system in myelodysplastic syndromes and acute myeloid leukemia.
Review in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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
1 citing paper in PubMed.
- Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The insulin-like growth factor (IGF) signaling system comprises functionally specific ligands (IGF-I and IGF-II), receptor (IR), and binding proteins (IGFBP). IGFs are activated by binding to their receptor, IGF-IR, which is a tyrosine kinase receptor. This activation initiates signaling cascades such as PI3K/Akt and MAPK/ErK pathways, which are essential for cell proliferation, differentiation, and survival. Growing evidence links the IGF system to various hematological disorders, yet comprehensive reviews on its role in Myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) are limited. To advance understanding in this area, we aim to summarize the emerging evidence on the involvement of IGF signaling in the pathogenesis of MDS and AML. Specifically, we highlight how dysregulation of IGF-I, IGF-IR, and IGFBPs contributes to disease progression, encompassing clonal hematopoietic abnormalities, ineffective hematopoiesis in MDS, and the development of AML. The potential therapeutic implications of targeting the IGF signaling pathway, including the role of NVP-AEW541 and NVP-ADW742 effectively suppressing AML cell proliferation and enhancing chemotherapy sensitivity, are also explored. By integrating current findings, this review provides novel insights into the mechanistic role of IGF signaling in MDS and AML and its therapeutic implications, thereby guiding future research and potential clinical applications. Given the challenges, such as pathway redundancy and therapy resistance, further investigations are necessary to validate IGF-targeted therapies and optimize their clinical utility in hematologic malignancies.
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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 Socratic graph.