ReviewCancer medicine2025
Tropomyosin 3 Gene Fusions in Cancers: From Mechanisms to Treatments-A Comprehensive Review.
Review in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Exosomal miR-145-5p inhibits papillary thyroid cancer by targetingOncology letters · 2026Article
- Tropomyosin 3 Gene Fusions in Cancers: From Mechanisms to Treatments-A Comprehensive Review.Cancer medicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundTropomyosin 3 (TPM3), one of the four tropomyosin genes, is predominantly expressed in eukaryotic cells. As a crucial regulatory protein, TPM3 associates with actin within thin myofilaments, thereby playing an essential role in the regulation of muscle contraction. Beyond its fundamental function in muscle physiology, TPM3 is implicated in oncogenesis.
objectiveThis review elucidates the molecular mechanisms underpinning TPM3 gene fusions, delineates the tumor types associated with these fusions, and examines their clinical implications.
findingsGene fusions such as TPM3-NTRK1, TPM3-ALK, and TPM3-ROS1 have been identified as oncogenic drivers in various cancers. These fusions promote constitutive activation of tyrosine kinases, disrupt normal cellular signaling, and consequently accelerate tumorigenesis. Malignancies harboring TPM3 fusions encompass several tumor categories. With the advent of tyrosine kinase inhibitors (TKIs) targeting NTRK1, ALK, and ROS1 fusions, these rearrangements have gained significant therapeutic relevance. However, resistance mechanisms and tumor heterogeneity pose ongoing challenges to targeted therapy.
conclusionBy synthesizing current evidence, this review aims to provide insights into the diagnostic, prognostic, and therapeutic landscape of TPM3-related gene fusions, fostering advancements in precision oncology.
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.