ArticleCancer cell2026
The landscape of structural variation in pediatric cancer.
Article in Cancer cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Clustered structural variant hotspots enable oncogenic addiction and plasticity in osteosarcoma.bioRxiv : the preprint server for biology · 2026Article
- Unsupervised Deep Representation Learning and Probabilistic Clustering for the Systems-Level Discovery of Germline Mutation Signatures in Pediatric Cancers.Biomedicines · 2026Article
- IRS4 is a PI3K-activating cancer dependency up-regulated through DNA rearrangements or epigenetic mechanisms in multiple solid tumors.Science advances · 2026Article
- A hybrid Ornstein-Uhlenbeck-Branching framework unifies microbial and pediatric tumor evolution.Frontiers in oncology · 2026Article
- Fast and sensitive detection of targeted gene fusions using frequency minimizers and fuzzy pattern matching with Fuzzion2.Cell reports methods · 2025Article
Corrections and comments
- Update of
Authors and funding
17 authors.
Funding
Abstract
Structural variants (SVs) account for over 60% of pediatric cancer driver variants. Pan-cancer analyses on 1,616 pediatric and 2,203 adult whole genomes show that pediatric SV burden varies ∼100-fold across cancer types, is reduced 6- to 16-fold compared to adult brain and solid tumors, but is comparable in hematological malignancies. The top-ranked SV-disrupted genes are drivers in pediatric cancers and fragile sites in adult cancers. Recurrent SV hotspots near RAG recombination signal sequences disrupt immune loci and driver genes in pediatric acute lymphoblastic leukemias, but immune loci exclusively in adult lymphoid cancers. Ten extracted SV signatures implicate RAG-mediated mutagenesis as a potential etiology for COSMIC SV7 in lymphoid cancers, while clustering of spatiotemporally distinct samples from 13 patients reveals the ongoing evolutionary contributions of SVs to intra-tumor heterogeneity and driver selection. Our study expands the known scope of RAG-mediated mutagenesis, while the curated SV dataset can guide future research and clinical testing.
Indexed as
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.