ArticleNPJ precision oncology2022
Drivers of genomic loss of heterozygosity in leiomyosarcoma are distinct from carcinomas.
Article in NPJ precision oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- A multicenter, randomized, non-comparative, phase II study of nivolumab ± ipilimumab for patients with metastatic sarcoma (Alliance A091401): expansion cohorts and correlative analyses.Journal for immunotherapy of cancer · 2024Trial
- Current Evidence for Circulating Tumor DNA in Sarcoma: Challenges and Opportunities for Clinical Application.Journal of surgical oncology · 2026Review
- E2F1-mediatedCytoJournal · 2025Article
- Clinical actionability of BRCA2 alterations in uterine leiomyosarcoma: a molecular tumor board case report and a cBioPortal comprehensive analysis.The oncologist · 2024Article
- Loss of the DNA Repair Gene RNase H2 Identifies a Unique Subset of DDR-Deficient Leiomyosarcomas.Molecular cancer therapeutics · 2024Article
- Gene partners of the EWSR1 fusion may represent molecularly distinct entities.Translational oncology · 2023Article
- Mutations in Homologous Recombination Genes and Loss of Heterozygosity Status in Advanced-Stage Breast Carcinoma.Cancers · 2023Article
- Feasibility of Longitudinal ctDNA Assessment in Patients with Uterine and Extra-Uterine Leiomyosarcoma.Cancers · 2022Article
- Drivers of genomic loss of heterozygosity in leiomyosarcoma are distinct from carcinomas.NPJ precision oncology · 2022Article
- Long-Time Progression-Free Survival with Trabectedin in Chemorefractory Metastatic Leiomyosarcoma of the Retroperitoneum: A Case Report.Case reports in oncologyArticle
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Leiomyosarcoma (LMS) is a rare, aggressive, mesenchymal tumor. Subsets of LMS have been identified to harbor genomic alterations associated with homologous recombination deficiency (HRD); particularly alterations in BRCA2. Whereas genomic loss of heterozygosity (gLOH) has been used as a surrogate marker of HRD in other solid tumors, the prognostic or clinical value of gLOH in LMS (gLOH-LMS) remains poorly defined. We explore the genomic drivers associated with gLOH-LMS and their clinical import. Although the distribution of gLOH-LMS scores are similar to that of carcinomas, outside of BRCA2, there was no overlap with previously published gLOH-associated genes from studies in carcinomas. We note that early stage tumors with elevated gLOH demonstrated a longer disease-free interval following resection in LMS patients. Taken together, and despite similarities to carcinomas in gLOH distribution and clinical import, gLOH-LMS are driven by different genomic signals. Additional studies will be required to isolate and confirm the unique differences in biological factors driving these differences.
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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.