ArticleBJC reports2026
Immune remodeling and myeloid signature in the bone marrow niche of MYCN-driven neuroblastoma.
Article in BJC reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHigh-risk MYCN-amplified neuroblastoma is associated with a dire prognosis and often metastasizes to the bone marrow. However, systemic immune remodeling and its effect on the bone marrow niche remain unclear.
methodsHarnessing single-cell RNA sequencing, we compare the bone marrow immune cell landscape of wild-type (WT) mice and TH-MYCN transgenic mice.
resultsTH-MYCN mice showed increased neutrophils and Cd300e+ myeloid cells, and reduced developing B cells, mirroring our findings in human neuroblastoma bone marrow metastases. Ligand-receptor analysis revealed enrichment of ADGRG and SEMA4 signaling pathways in TH-MYCN bone marrow, highlighting Tgm2-Adgrg1, Sema4D-Plxnb2, and Sema4D-Cd72 interactions as potential immune modulators. In contrast, CD45 and CEACAM pathways were prominent in WT mice, suggesting context-specific immune regulation. A distinct Cd300e+ Pecam1+ myeloid population enriched in TH-MYCN mice, exhibited a gene signature, including Fabp4, Ear2 (Nr2f6), and Treml4, genes associated with neuroblastoma staging and poor survival. FABP4+ macrophages, enriched in MYCN-amplified neuroblastoma relapse, have been implicated in enhancing tumor cell migration, invasion, and growth.
conclusionsOur data reveals the distant influence of primary tumors on bone marrow immune composition and signaling. These insights into bone marrow immune remodeling highlight FABP4+ macrophages and semaphorin signaling as potential immunotherapeutic targets to disrupt neuroblastoma progression.
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.