ArticleCancer2021
Relationships between highly recurrent tumor suppressor alterations in 489 leiomyosarcomas.
Article in Cancer, 2021. 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
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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
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
16 citing papers in PubMed, 34 citations in OpenAlex.
- Clinicopathological and molecular features of uterine smooth muscle tumours in patients with Li-Fraumeni syndrome.Histopathology · 2026Article
- Therapeutic Vulnerabilities of the Key Genetic Drivers in Leiomyosarcoma.Medical sciences (Basel, Switzerland) · 2026Review
- Leiomyosarcoma Therapeutic Approaches and Future Directions.Hematology/oncology clinics of North America · 2025Review
- Untangling the Role of MYC in Sarcomas and Its Potential as a Promising Therapeutic Target.International journal of molecular sciences · 2025Review
- Comprehensive mutational profiling identifies new driver events in cutaneous leiomyosarcoma.The British journal of dermatology · 2025Article
- Molecular Heterogeneity in Leiomyosarcoma and Implications for Personalised Medicine.Current treatment options 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
- Secondary leiomyosarcoma of the nasal cavity in a treated patient with possible hereditary retinoblastoma with germline reciprocal translocation of RB1 and DMXL1 and somatic TP53 mutation: A case report.Molecular and clinical oncology · 2023Article
- Not All Leiomyosarcomas Are the Same: How to Best Classify LMS.Current treatment options in oncology · 2023Review
- Molecular-Based Immunohistochemical Algorithm for Uterine Leiomyosarcoma Diagnosis.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2023Article
- Review
- Concurrent inhibition of CDK2 adds to the anti-tumour activity of CDK4/6 inhibition in GIST.British journal of cancer · 2022Article
- Adult NTRK-rearranged spindle cell neoplasms of the viscera: with an emphasis on rare locations and heterologous elements.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022Article
- 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
- Role of Homologous Recombination Repair (HRR) Genes in Uterine Leiomyosarcomas: A Retrospective Analysis.Cancers · 2022Article
- Leiomyosarcoma: Does Location of Primary Help to Determine the Best Systemic Therapy Options?Current treatment options in oncology · 2021Review
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 4 countries.
Funding
Abstract
backgroundLeiomyosarcoma (LMS) is the most common soft tissue and uterine sarcoma, but no standard therapy is available for recurrent or metastatic LMS. TP53, p16/RB1, and PI3K/mTOR pathway dysregulations are recurrent events, and some LMS express estrogen receptor (ER) and/or progesterone receptor (PR). To characterize relationships between these pathway perturbations, the authors evaluated protein expression in soft tissue and uterine nonprimary leiomyosarcoma (np-LMS), including local recurrences and distant metastases.
methodsTP53, RB1, p16, and PTEN expression aberrations were determined by immunohistochemistry (IHC) in tissue microarrays (TMAs) from 227 np-LMS and a comparison group of 262 primary leiomyosarcomas (p-LMS). Thirty-five of the np-LMS had a matched p-LMS specimen in the TMAs. Correlative studies included differentiation scoring, ER and PR IHC, and CDKN2A/p16 fluorescence in situ hybridization.
resultsDysregulation of TP53, p16/RB1, and PTEN was demonstrated in 90%, 95%, and 41% of np-LMS, respectively. PTEN inactivation was more common in soft tissue np-LMS than uterine np-LMS (55% vs 31%; P = .0005). Moderate-strong ER expression was more common in uterine np-LMS than soft tissue np-LMS (50% vs 7%; P < .0001). Co-inactivation of TP53 and RB1 was found in 81% of np-LMS and was common in both soft tissue and uterine np-LMS (90% and 74%, respectively). RB1, p16, and PTEN aberrations were nearly always conserved in p-LMS and np-LMS from the same patients.
conclusionsThese studies show that nearly all np-LMS have TP53 and/or RB1 aberrations. Therefore, therapies targeting cell cycle and DNA damage checkpoint vulnerabilities should be prioritized for evaluations in LMS.
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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.