ReviewTargeted oncology2025
MYC as a Target for Cancer Treatment: from Undruggable to Druggable?
Review in Targeted oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed.
- RareJTO clinical and research reports · 2026Article
- Pinoresinol as a Potential c-Myc Complex Modulator: An In Silico Study.Current issues in molecular biology · 2026Article
- Informing agent-based models with spatial data using convolutional autoencoders.Bioinformatics (Oxford, England) · 2026Article
- MYC in Oncogenesis and Therapeutic Implications.MedComm · 2026Review
- Transcription factor targeting strategies in cancer: mechanisms, challenges and cutting-edge progress.Acta pharmacologica Sinica · 2026Review
- Targeting the Undruggable: Deep Learning-Driven Design of Peptide Therapeutics in Cancer.Pharmaceuticals (Basel, Switzerland) · 2026Review
- RiboScreenBiomedicines · 2026Review
- Understanding and Overcoming Osteosarcoma Heterogeneity.Biomolecules · 2026Review
- MYC_V1-Related Genes Affect Gastric Cancer Proliferation by Regulating Energy Metabolism and Analysis of Therapeutic Targets.International journal of molecular sciences · 2026Article
- Ribosome biogenesis bottlenecks reveal vulnerabilities in cancer.bioRxiv : the preprint server for biology · 2026Article
- Copper Transporter 1‑Mediated Deregulation of Copper Homeostasis Impacts MYC and Oxidative Phosphorylation Pathways and Increases the Sensitivity of Tumor Cells to Complex I Inhibitors.ACS pharmacology & translational science · 2026Article
- Molecularly Targeted Therapies in Oncology: Mechanisms, Resistance, and Combination Strategies.Molecules (Basel, Switzerland) · 2026Review
- De Novo Protein Design Enables Targeting of Intractable Oncogenic Protein-Protein Interfaces.Biologics (Basel, Switzerland) · 2026Article
- Heat Stress Modulates WDR5-Mediated H3K4me3 Modification to Induce Melanogenesis via Activating CX3CL1/CX3CR1 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- MYC at the tumor-immune interface: mechanisms of immune escape and immunotherapy resistance.Frontiers in immunology · 2026Review
- Small B-cell lymphoma highly suspicious for splenic marginal zone lymphoma withFrontiers in immunology · 2026Review
- De novo protein design enables targeting of intractable oncogenic interfaces.bioRxiv : the preprint server for biology · 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MYC is one of the most frequently altered genes in cancer with an estimated 70% prevalence of deregulation. Deregulated MYC is believed to promote cancer formation/progression via multiple mechanisms including tumour cell intrinsic mechanisms, altering the tumour microenvironment and promoting host immune suppression. Owing to the high prevalence of alterations and its causative role in tumorigenesis, MYC is a highly attractive target for new anticancer therapies. However, as MYC lacks a readily identifiably pocket for potential low molecular weight inhibitors and is predominantly located in the cell nucleus, it has proved difficult to target using standard pharmacological approaches. Recently, however, these problems appear to have been successfully resolved, with the discovery of promising anti-MYC compounds such as Omomyc or MYCi975. Both Omomyc and MYCi975 exhibit anti-cancer activity in several different animal models, with apparently little short-term toxicity. Furthermore, consistent with the ability of MYC to promote a pro-tumour microenvironment and induce immune evasion, treatment with Omomyc or MYCi975 was shown to increase uptake of anti-tumour lymphocytes and enhance response to immunotherapy. Currently, at least five anti-MYC compounds are being evaluated for potential anti-cancer activity in clinical trials. Results from a phase I trial with OMO-103 (a form of Omomyc) suggest that the inhibitor is well tolerated, with most of its adverse effects being at grade 1 level. Evidence of target inhibition was the finding of decreased expression of multiple MYC regulated genes.
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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.