ReviewClinical and translational medicine2025
Telomere-metabolism-immunity axis in sarcoma: Immune evasion mechanisms and therapeutic strategies.
Review in Clinical and translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Telomere-metabolism-immunity axis in sarcoma: Immune evasion mechanisms and therapeutic strategies.Clinical and translational medicine · 2025Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Sarcomas are a heterogeneous group of mesenchymal malignancies with poor prognosis and limited response to standard therapies, including immune checkpoint inhibitors (ICIs). Tumour-intrinsic factors-such as telomere maintenance mechanisms (TMMs) and metabolic reprogramming-play central roles in driving immune evasion and therapeutic resistance. Telomerase activation and alternative lengthening of telomeres sustain replicative immortality while influencing the tumour immune microenvironment. In parallel, metabolic adaptations, including glutamine dependency and arginine auxotrophy, further suppress antitumour immunity. Together, TMMs and metabolism form an integrated axis that shapes immune modulation and treatment outcomes. Recent advances-ranging from telomerase-based vaccines and TMM-targeted immunotherapies to metabolic modulators combined with ICIs-demonstrate the translational promise of targeting this axis. This review synthesises current knowledge on telomere‒metabolism crosstalk in sarcomas, highlights its impact on immunotherapy response, and outlines future directions for biomarker-driven, combinatorial strategies to overcome resistance and improve patient outcomes. KEY POINTS: Telomere maintenance mechanisms (telomerase reverse transcriptase and alternative lengthening of telomeres) reprogram metabolism and dampen innate immune sensing in sarcomas. Metabolic rewiring (glutamine addiction, glycolysis and fatty acid oxidation) fosters T-cell dysfunction and myeloid-derived suppressor cell accumulation. Targeting the telomere‒metabolism‒immunity axis offers strategies to overcome immunotherapy resistance.
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