ArticleMolecular cancer research : MCR2020
Oncogenic Gene-Expression Programs in Leiomyosarcoma and Characterization of Conventional, Inflammatory, and Uterogenic Subtypes.
Article in Molecular cancer research : MCR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Leiomyosarcoma of the abdomen and retroperitoneum; a systematic review.Frontiers in surgery · 2024Pooled it
- Therapeutic Vulnerabilities of the Key Genetic Drivers in Leiomyosarcoma.Medical sciences (Basel, Switzerland) · 2026Review
- 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
- An Update on Uterine Smooth Muscle Tumors: Is It a Leiomyoma, a STUMP, or a Leiomyosarcoma?Biomedicines · 2026Review
- Molecular carcinogenesis and genetic insights in leiomyosarcoma: involvement of PI3K/AKT/mTOR/MAPK/ERK pathway.American journal of cancer research · 2026Review
- Loss ofCurrent issues in molecular biology · 2025Article
- Proteomic features of soft tissue tumours in adolescents and young adults.Communications medicine · 2024Article
- Molecular Heterogeneity in Leiomyosarcoma and Implications for Personalised Medicine.Current treatment options in oncology · 2024Review
- Comprehensive Immune Profiling Unveils a Subset of Leiomyosarcoma with "Hot" Tumor Immune Microenvironment.Cancers · 2023Article
- The proteomic landscape of soft tissue sarcomas.Nature communications · 2023Article
- Downregulation of miR‑10b‑5p facilitates the proliferation of uterine leiomyosarcoma cells: A microRNA sequencing‑based approach.Oncology reports · 2023Article
- The Functional Role and Regulatory Mechanism of FTO mInternational journal of molecular sciences · 2023Article
- Not All Leiomyosarcomas Are the Same: How to Best Classify LMS.Current treatment options in oncology · 2023Review
- Article
- Therapeutic advances in leiomyosarcoma.Frontiers in oncology · 2023Review
- Preclinical Modeling of Leiomyosarcoma Identifies Susceptibility to Transcriptional CDK Inhibitors through Antagonism of E2F-Driven Oncogenic Gene Expression.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Gamma Secretase Inhibitors as Potential Therapeutic Targets for Notch Signaling in Uterine Leiomyosarcoma.International journal of molecular sciences · 2022Article
- Aberrant Activation of Cell-Cycle-Related Kinases and the Potential Therapeutic Impact of PLK1 or CHEK1 Inhibition in Uterine Leiomyosarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Computational Discovery of Cancer Immunotherapy Targets by Intercellular CRISPR Screens.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Leiomyosarcoma (LMS) is a mesenchymal neoplasm with complex copy-number alterations and characteristic loss of tumor suppressor genes without known recurrent activating mutations. Clinical management of advanced LMS relies on chemotherapy and complementary palliative approaches, and research efforts to date have had limited success identifying clinically actionable biomarkers or targeted therapeutic vulnerabilities. To explore the biological underpinning of LMS, we evaluated gene-expression patterns of this disease in comparison with diverse sarcomas, nonmesenchymal neoplasms, and normal myogenic tissues. We identified a recurrent gene-expression program in LMS, with evidence of oncogenic evolution of an underlying smooth-muscle lineage-derived program characterized by activation of E2F1 and downstream effectors. Recurrently amplified or highly expressed genes in LMS were identified, including IGF1R and genes involved in retinoid signaling pathways. Though the majority of expressed transcripts were conserved across LMS samples, three separate subtypes were identified that were enriched for muscle-associated transcripts (conventional LMS), immune markers (inflammatory LMS), or a uterine-like gene-expression program (uterogenic LMS). Each of these subtypes expresses a unique subset of genes that may be useful in the management of LMS: IGF1R was enriched in conventional LMS, worse disease-specific survival was observed in inflammatory LMS, and prolactin was elaborated by uterogenic LMS. These results extend our understanding of LMS biology and identify several strategies and challenges for further translational investigation. IMPLICATIONS: LMS has a recurrent oncogenic transcriptional program and consists of molecular subtypes with biological and possible clinical implications.
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