ArticleCancer2025
Intratumoral heterogeneity of cancer driver genomic alterations in myxoid liposarcomas.
Article in Cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Molecular and Immune Mechanisms Governing Cancer Metastasis, Including Dormancy, Microenvironmental Niches, and Tumor-Specific Programs.International journal of molecular sciences · 2026Review
- KNTC1 and PRC1 define an immunosuppressive microenvironment and poor prognosis in liposarcoma.European journal of medical research · 2026Article
- Intratumoral heterogeneity of cancer driver genomic alterations in myxoid liposarcomas.Cancer · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
backgroundMyxoid liposarcomas (MLS) are rare malignant mesenchymal tumors characterized by specific translocations t(12;16) and t(12;22) with limited additional driver mutations, most notably in PIK3CA and the TERT promoter. PIK3CA is considered a promising therapeutic target. However, effective treatments require the uniform presence of mutation throughout the tumor. Therefore, this study evaluated intratumoral heterogeneity of driver mutations in MLS.
methodsIn total, 170 samples from 20 tumors (12 patients) were analyzed using an MLS-specific next-generation sequencing (NGS) panel. This included detecting the t(12;16) and t(12;22) translocations and known driver mutations.
resultsPatient-specific t(12;16) or t(12;22) translocations were detected in all 20 tumors (159 of 170 samples; 94%) and remained identical in primary tumors, recurrences, and metastases. TERT promoter mutations were identified in 17 of 20 tumors (85%) and were distributed similarly across samples. In contrast, PIK3CA mutations were present in only 66 of 170 samples (39%), with these and the remaining driver mutations localized only in subclones within individual tumors.
conclusionsTherapies that target PIK3CA are unlikely to succeed because of its limited subclonal distribution. In contrast, the ubiquitous presence of t(12;16), t(12;22), and TERT promoter mutations across MLS tumors suggests that these are more effective therapeutic targets for future treatment strategies.
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.