ReviewRedox biology2019
Genetics, epigenetics and redox homeostasis in rhabdomyosarcoma: Emerging targets and therapeutics.
Review in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 33 citations in OpenAlex.
- Catalase Defines Radiotherapy Resistance and a Therapeutic Vulnerability in Rhabdomyosarcoma.International journal of molecular sciences · 2026Article
- Nanotechnology-mediated strategies for skeletal muscle repair and regeneration: targeted intervention, functional remodeling, and translational challenges.Journal of nanobiotechnology · 2026Review
- Targeting the IRE1α-XBP1 signaling axis impairs tumor growth and promotes myogenic differentiation in rhabdomyosarcoma.Communications biology · 2026Article
- Targeting the IRE1α-XBP1 signaling axis impairs tumor growth and promotes myogenic differentiation in rhabdomyosarcoma.bioRxiv : the preprint server for biology · 2026Article
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- Lnc-PSMA8-1 activated by GEFT promotes rhabdomyosarcoma progression via upregulation of mTOR expression by sponging miR-144-3p.BMC cancer · 2024Article
- MEK and MCL-1 sequential inhibition synergize to enhance rhabdomyosarcoma treatment.Cell death discovery · 2022Article
- Nuclear TIGAR mediates an epigenetic and metabolic autoregulatory loopActa pharmaceutica Sinica. B · 2022Article
- Bromodomain Inhibitor JQ1 Provides Novel Insights and Perspectives in Rhabdomyosarcoma Treatment.International journal of molecular sciences · 2022Article
- Co-targeting MCL-1 and ERK1/2 kinase induces mitochondrial apoptosis in rhabdomyosarcoma cells.Translational oncology · 2022Article
- Radioresistance in rhabdomyosarcomas: Much more than a question of dose.Frontiers in oncology · 2022Review
- Protein Arginine Methyltransferase (PRMT) Inhibitors-AMI-1 and SAH Are Effective in Attenuating Rhabdomyosarcoma Growth and Proliferation in Cell Cultures.International journal of molecular sciences · 2021Article
- Metabolic landscapes in sarcomas.Journal of hematology & oncology · 2021Review
- Dihydroartemisinin Inhibits mTORC1 Signaling by Activating the AMPK Pathway in Rhabdomyosarcoma Tumor Cells.Cells · 2021Article
- Vincetoxicum arnottianum modulates motility features and metastatic marker expression in pediatric rhabdomyosarcoma by stabilizing the actin cytoskeleton.BMC complementary medicine and therapies · 2021Article
- Emerging Role and Mechanism of circRNAs in Pediatric Malignant Solid Tumors.Frontiers in genetics · 2021Review
- EHMT2 epigenetically suppresses Wnt signaling and is a potential target in embryonal rhabdomyosarcoma.eLife · 2020Article
- Survival and prognostic analysis of preoperative indicators in patients undergoing surgical resections with rhabdomyosarcoma.Medicine · 2020Article
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma accounting for 5-8% of malignant tumours in children and adolescents. Children with high risk disease have poor prognosis. Anti-RMS therapies include surgery, radiation and combination chemotherapy. While these strategies improved survival rates, they have plateaued since 1990s as drugs that target differentiation and self-renewal of tumours cells have not been identified. Moreover, prevailing treatments are aggressive with drug resistance and metastasis causing failure of several treatment regimes. Significant advances have been made recently in understanding the genetic and epigenetic landscape in RMS. These studies have identified novel diagnostic and prognostic markers and opened new avenues for treatment. An important target identified in high throughput drug screening studies is reactive oxygen species (ROS). Indeed, many drugs in clinical trials for RMS impact tumour progression through ROS. In light of such emerging evidence, we discuss recent findings highlighting key pathways, epigenetic alterations and their impacts on ROS that form the basis of developing novel molecularly targeted therapies in RMS. Such targeted therapies in combination with conventional therapy could reduce adverse side effects in young survivors and lead to a decline in long-term morbidity.
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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 Socratic graph.