ArticleNature genetics2014
Dystrophin is a tumor suppressor in human cancers with myogenic programs.
Article in Nature genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 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
105 citing papers in PubMed, 162 citations in OpenAlex.
- Precision therapeutic strategies for advanced gastrointestinal stromal tumors.Cancer metastasis reviews · 2026Review
- Multiomic Landscape of Gastrointestinal Stromal Tumors in a Real-World Patient Cohort of 1,427 Cases.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Exploring Dystrophin Expression and Mutations in theInternational journal of molecular sciences · 2026Article
- Frequent expression of aberrant chimeric Cdkn2a transcripts in mouse models of muscular dystrophy.Scientific reports · 2026Article
- Cell therapy for Duchenne muscular dystrophy: promises, challenges, and controversies.Cellular and molecular life sciences : CMLS · 2025Review
- Is dystrophin immunogenicity a barrier to advancing gene therapy for Duchenne muscular dystrophy?Gene therapy · 2025Review
- Deficient Astrocyte Homeostatic Support Contributes to Brain Impairment in Duchenne Muscular Dystrophy.Neurochemical research · 2025Review
- Molecular basis of proteolytic cleavage regulation by the extracellular matrix receptor dystroglycan.Structure (London, England : 1993) · 2024Article
- Genomic and transcriptomic landscape of human gastrointestinal stromal tumors.Nature communications · 2024Article
- Machine-learning and scRNA-Seq-based diagnostic and prognostic models illustrating survival and therapy response of lung adenocarcinoma.Genes and immunity · 2024Article
- Differential expression ofTranslational lung cancer research · 2024Article
- Pathologic diagnosis and molecular features of gastrointestinal stromal tumors: a mini-review.Frontiers in oncology · 2024Review
- Hyper-Dependence on NHEJ Enables Synergy between DNA-PK Inhibitors and Low-Dose Doxorubicin in Leiomyosarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Chromosomal instability and a deregulated cell cycle are intrinsic features of high-risk gastrointestinal stromal tumours with a metastatic potential.Molecular oncology · 2023Article
- Therapeutic approaches for Duchenne muscular dystrophy.Nature reviews. Drug discovery · 2023Review
- Replication stress in mammalian embryo development, differentiation, and reprogramming.Trends in cell biology · 2023Review
- Telomere-Associated Gene Signatures Correlate with Prognosis, Tumor Microenvironment, and Chemosensitivity in Breast Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2023Article
- Analysis of the Mutational Landscape of Osteosarcomas Identifies Genes Related to Metastasis and Prognosis and Disrupted Biological Pathways of Immune Response and Bone Development.International journal of molecular sciences · 2023Article
- Whole-genome and Epigenomic Landscapes of Malignant Gastrointestinal Stromal Tumors HarboringCancer research communications · 2023Article
- Article
45 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
20 authors at 9 institutions in 1 country.
Funding
Abstract
Many common human mesenchymal tumors, including gastrointestinal stromal tumor (GIST), rhabdomyosarcoma (RMS) and leiomyosarcoma (LMS), feature myogenic differentiation. Here we report that intragenic deletion of the dystrophin-encoding and muscular dystrophy-associated DMD gene is a frequent mechanism by which myogenic tumors progress to high-grade, lethal sarcomas. Dystrophin is expressed in the non-neoplastic and benign counterparts of GIST, RMS and LMS tumors, and DMD deletions inactivate larger dystrophin isoforms, including 427-kDa dystrophin, while preserving the expression of an essential 71-kDa isoform. Dystrophin inhibits myogenic sarcoma cell migration, invasion, anchorage independence and invadopodia formation, and dystrophin inactivation was found in 96%, 100% and 62% of metastatic GIST, embryonal RMS and LMS samples, respectively. These findings validate dystrophin as a tumor suppressor and likely anti-metastatic factor, suggesting that therapies in development for muscular dystrophies may also have relevance in the treatment of cancer.
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.