ArticleNature communications2021
Lineage-defined leiomyosarcoma subtypes emerge years before diagnosis and determine patient survival.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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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
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Who cites it
38 citing papers in PubMed, 60 citations in OpenAlex.
- Clinical Heterogeneity and Survival Disparities in Leiomyosarcoma: An Exploratory Single-Center Retrospective Observational Study.Journal of clinical medicine · 2026Article
- Therapeutic Vulnerabilities of the Key Genetic Drivers in Leiomyosarcoma.Medical sciences (Basel, Switzerland) · 2026Review
- Current Evidence for Circulating Tumor DNA in Sarcoma: Challenges and Opportunities for Clinical Application.Journal of surgical oncology · 2026Review
- Exploring Dystrophin Expression and Mutations in theInternational journal of molecular sciences · 2026Article
- Spatially-Resolved Multiomic Atlas of Leiomyosarcoma Identifies Two Clinically Relevant Epigenetically-Driven Cell States.bioRxiv : the preprint server for biology · 2026Article
- Predicting immunotherapy benefit in leiomyosarcoma through active chromatin cfDNA profiling.NPJ precision oncology · 2026Article
- Transcriptomic Subgroups in Soft Tissue Tumors Correlate with Morphologic Subtype, Genomic Features, and Outcome.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Clinical Characteristics of Complex Karyotype Soft Tissue Sarcomas: A Single-Institution Cohort Study.Medicina (Kaunas, Lithuania) · 2026Article
- Molecular carcinogenesis and genetic insights in leiomyosarcoma: involvement of PI3K/AKT/mTOR/MAPK/ERK pathway.American journal of cancer research · 2026Review
- Transcriptomic-Based Classification Identifies Prognostic Subtypes and Therapeutic Strategies in Soft Tissue Sarcomas.Cancers · 2025Article
- Review
- Evolutionary Pressures Shape Undifferentiated Pleomorphic Sarcoma Development and Radiotherapy Response.Cancer research · 2025Article
- Genomic characterization and histologic analysis of uterine leiomyosarcoma arising from leiomyoma with bizarre nuclei.The Journal of pathology · 2025Article
- Chronification of metastatic leiomyosarcoma in 9 lines of therapy by precision oncology: a case report and review of the literature.Frontiers in oncology · 2025Article
- Novel Therapeutics in Soft Tissue Sarcoma.Cancers · 2024Review
- Dysregulation of miRNAs in Soft Tissue Sarcomas.Cells · 2024Review
- Molecular basis of proteolytic cleavage regulation by the extracellular matrix receptor dystroglycan.Structure (London, England : 1993) · 2024Article
- Advancement in Multi-omics approaches for Uterine Sarcoma.Biomarker research · 2024Review
- The Impact of Li-Fraumeni and Germline Retinoblastoma Mutations on Leiomyosarcoma Initiation, Outcomes, and Genetic Testing Recommendations.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Inhibition of Aberrantly Overexpressed Polo-like Kinase 4 Is a Potential Effective Treatment for DNA Damage Repair-Deficient Uterine Leiomyosarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
Corrections and comments
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Authors and funding
31 authors at 7 institutions in 3 countries.
Funding
Abstract
Leiomyosarcomas (LMS) are genetically heterogeneous tumors differentiating along smooth muscle lines. Currently, LMS treatment is not informed by molecular subtyping and is associated with highly variable survival. While disease site continues to dictate clinical management, the contribution of genetic factors to LMS subtype, origins, and timing are unknown. Here we analyze 70 genomes and 130 transcriptomes of LMS, including multiple tumor regions and paired metastases. Molecular profiling highlight the very early origins of LMS. We uncover three specific subtypes of LMS that likely develop from distinct lineages of smooth muscle cells. Of these, dedifferentiated LMS with high immune infiltration and tumors primarily of gynecological origin harbor genomic dystrophin deletions and/or loss of dystrophin expression, acquire the highest burden of genomic mutation, and are associated with worse survival. Homologous recombination defects lead to genome-wide mutational signatures, and a corresponding sensitivity to PARP trappers and other DNA damage response inhibitors, suggesting a promising therapeutic strategy for LMS. Finally, by phylogenetic reconstruction, we present evidence that clones seeding lethal metastases arise decades prior to LMS diagnosis.
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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.