ArticleMolecular oncology2021
Intratumoral immunosuppression profiles in 11q-deleted neuroblastomas provide new potential therapeutic targets.
Article in Molecular oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Reprogramming the neuroblastoma tumor immune microenvironment to enhance GPC2 CAR T cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Targeting Pathways in Neuroblastoma: Advances in Treatment Strategies and Clinical Outcomes.International journal of molecular sciences · 2025Review
- The regulatory role of immune microenvironment-related cells and pathways in the pathogenesis of keloids.Frontiers in immunology · 2025Review
- Liquidhope: methylome and genomic profiling from very limited quantities of plasma-derived DNA.Briefings in bioinformatics · 2023Article
- Divergent HLA variations and heterogeneous expression but recurrent HLA loss-of- heterozygosity and commonFrontiers in immunology · 2023Article
- Recent Advances in Pediatric Cancer Research.Cancer research · 2021Review
- Molecular Genetics in Neuroblastoma Prognosis.Children (Basel, Switzerland) · 2021Review
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-risk neuroblastoma (NB) patients with 11q deletion frequently undergo late but consecutive relapse cycles with fatal outcome. To date, no actionable targets to improve current multimodal treatment have been identified. We analyzed immune microenvironment and genetic profiles of high-risk NB correlating with 11q immune status. We show in two independent cohorts that 11q-deleted NB exhibits various immune inhibitory mechanisms, including increased CD4+ resting T cells and M2 macrophages, higher expression of programmed death-ligand 1, interleukin-10, transforming growth factor-beta-1, and indoleamine 2,3-dioxygenase 1 (P < 0.05), and also higher chromosomal breakages (P ≤ 0.02) and hemizygosity of immunosuppressive miRNAs than MYCN-amplified and other 11q-nondeleted high-risk NB. We also analyzed benefits of maintenance treatment in 83 high-risk stage M NB patients focusing on 11q status, either with standard anti-GD2 immunotherapy (n = 50) or previous retinoic acid-based therapy alone (n = 33). Immunotherapy associated with higher EFS (50 vs. 30, P = 0.028) and OS (72 vs. 52, P = 0.047) at 3 years in the overall population. Despite benefits from standard anti-GD2 immunotherapy in high-risk NB patients, those with 11q deletion still face poor outcome. This NB subgroup displays intratumoral immune suppression profiles, revealing a potential therapeutic strategy with combination immunotherapy to circumvent this immune checkpoint blockade.
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