ArticleiScience2025
MyoD is essential in rhabdomyosarcoma by promoting survival through differentiation and CYLD.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Paediatric Therapeutic Development Workshop on rhabdomyosarcoma.British journal of cancer · 2026Review
- HES3-dependent regulatory functions in development and fusion-positive rhabdomyosarcoma.bioRxiv : the preprint server for biology · 2026Article
- TAK1 is a key regulator of oncogenic signaling and differentiation blockade in rhabdomyosarcoma.Oncogene · 2026Article
- Changing Skin: The Prevalence, Impact, and Risks of Skin Bleaching Among African Women.Journal of racial and ethnic health disparities · 2025Review
- TAK1 is a key regulator of oncogenic signaling and differentiation blockade in rhabdomyosarcoma.bioRxiv : the preprint server for biology · 2025Article
- Meeting report: the inaugural muscle biology and cachexia conference at the University of Houston, May 18-20, 2025, Houston, Texas, USA.Frontiers in physiology · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Rhabdomyosarcoma (RMS) is the most common soft tissue cancer among children, characterized by a skeletal muscle lineage that is impaired from undergoing terminal differentiation. NF-κB is constitutively active in cancer cells and plays a critical role in cell survival. Although NF-κB is also activated in RMS, surprisingly, we find that these tumors are far less dependent on NF-κB for their survival. Instead, RMS cells survive, paradoxically, by being partially differentiated under the control of the myogenic transcription factor MyoD. Loss of MyoD, or cellular reprogramming, dedifferentiates RMS tumor cells and sensitizes their death under stress. MyoD enhances RMS survival by regulating DNA methyltransferases, which in turn suppresses the tumor suppressor and pro-apoptotic gene CYLD. From these findings, we propose that MyoD acts as an oncogene in RMS by enhancing survival through pro-differentiation and anti-cell death activities.
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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.