ArticleCell reports2022
Quantification of spatial subclonal interactions enhancing the invasive phenotype of pediatric glioma.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 18 citations in OpenAlex.
- A guide to understanding tumour evolution through the lens of population genetics.Nature reviews. Cancer · 2026Review
- Extracellular Vesicles in the Biology and Liquid Biopsy Diagnostics of Pediatric High-Grade Glioma - Emerging Findings and Opportunities.Journal of extracellular biology · 2026Review
- Subclonal β-catenin/YAP signaling heterogeneity accelerates ovarian cancer metastasis through a senescence-associated secretory phenotype.Cell death & disease · 2026Article
- Co-mapping clonal and transcriptional heterogeneity in somatic evolution via GoT-Multi.Cell genomics · 2026Article
- Non-invasive identification of mesenchymal glioblastoma using quantitative radiomic features from advanced diffusion MRI: a preclinical-to-clinical transfer learning strategy.European radiology experimental · 2025Article
- Small Extracellular Vesicles From Radioresistant H3K27M-Pediatric Diffuse Midline Glioma Cells Modulate Tumor Phenotypes and Radiation Response.Journal of extracellular vesicles · 2025Article
- Spatial analysis of a complete DIPG-infiltrated brainstem reveals novel ligand-receptor mediators of tumour-to-TME crosstalk.Acta neuropathologica communications · 2025Article
- Biomimetic Approach of Brain Vasculature Rapidly Characterizes Inter- and Intra-Patient Migratory Diversity of Glioblastoma.Small methods · 2024Article
- Modeling tumors as complex ecosystems.iScience · 2024Review
- 1q amplification and PHF19 expressing high-risk cells are associated with relapsed/refractory multiple myeloma.Nature communications · 2024Article
- A seven-step guide to spatial, agent-based modelling of tumour evolution.Evolutionary applications · 2024Review
- Modeling tumors as species-rich ecological communities.bioRxiv : the preprint server for biology · 2024Article
- Inhibition of exosome biogenesis affects cell motility in heterogeneous sub-populations of paediatric-type diffuse high-grade gliomas.Cell & bioscience · 2023Article
- Clinical and translational relevance of intratumor heterogeneity.Trends in cancer · 2023Review
- Toward a systems-level probing of tumor clonality.iScience · 2023Review
- Integration of quantitative methods and mathematical approaches for the modeling of cancer cell proliferation dynamics.American journal of physiology. Cell physiology · 2023Review
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 at 3 institutions in 2 countries.
Funding
Abstract
Diffuse midline gliomas (DMGs) are highly aggressive, incurable childhood brain tumors. They present a clinical challenge due to many factors, including heterogeneity and diffuse infiltration, complicating disease management. Recent studies have described the existence of subclonal populations that may co-operate to drive pro-tumorigenic processes such as cellular invasion. However, a precise quantification of subclonal interactions is lacking, a problem that extends to other cancers. In this study, we combine spatial computational modeling of cellular interactions during invasion with co-evolution experiments of clonally disassembled patient-derived DMG cells. We design a Bayesian inference framework to quantify spatial subclonal interactions between molecular and phenotypically distinct lineages with different patterns of invasion. We show how this approach could discriminate genuine interactions, where one clone enhanced the invasive phenotype of another, from those apparently only due to the complex dynamics of spatially restricted growth. This study provides a framework for the quantification of subclonal interactions in DMG.
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.