ArticleNPJ precision oncology2025
Natural history of SPP1 signaling in NF1 tumors.
Article in NPJ precision oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- EBV Triggers a Distinct Antiviral Response in HMC3 Cells.bioRxiv : the preprint server for biology · 2026Article
- Metabolic Alterations in Macrophage Subtypes Propel Immune and Stromal Remodeling in Neurofibroma's Malignant Progression.MedComm · 2026Article
- Emerging Molecular Insights and Therapeutic Directions in Neurofibromatosis Type 1 and NF2-Related Schwannomatosis.International journal of molecular sciences · 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
Abstract
Understanding the heterogeneity of Neurofibromatosis type 1 (NF1)-associated tumors and delineating the natural historical evolution of cell signaling are essential for interpreting tumor initiation, preventing tumor progression from benign plexiform neurofibromas (pNFs) to malignant peripheral nerve sheath tumors (MPNSTs), and engineering effective treatments. The neural crest-derived Schwann cell precursor (SCP)-like tumor population interacts with different cells in the tumor microenvironment (TME), particularly macrophages, continually shaping the intrinsic and extrinsic NF1 tumor heterogeneity. Through integrated analyses of single-cell RNA-seq (scRNA-seq) and spatial transcriptomics, we reveal that SPP1-CD44 signaling is initiated by SCP-like tumor cells in pNF, operating through autocrine mechanisms. However, in MPNST, a distinct subset of macrophages becomes the dominant SPP1 signaling source while the SCP-like cells maintain autocrine signaling. The role of SPP1 in tumorigenesis is validated by the significantly extended survival in the MPNST mouse model with cisNf1
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.