ArticleNature2008
Modelling Myc inhibition as a cancer therapy.
Article in Nature, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 474 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
474 citing papers in PubMed, 807 citations in OpenAlex.
- Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
- EphB4 inhibition defines a druggable synthetic-lethal vulnerability in MYC-driven triple-negative breast cancer.Cell death & disease · 2026Article
- MYC contributes to targeted therapy resistance in lung cancers driven by MET exon 14-skipping alteration.NPJ precision oncology · 2026Article
- An autochthonous CRISPR activation screening platform for characterizing tissue-specific oncogene selection.Cell reports. Medicine · 2026Article
- ARNT2 repression disrupts neuronal identity and promotes glioblastoma growth.Cell communication and signaling : CCS · 2026Article
- BEstimate: a computational tool for the design and interpretation of CRISPR base editing experiments.Genome biology · 2026Article
- Anthocyanin Derived NIR Fluorogenic Probe for Direct Visualization and Monitoring of DNA G‑Quadruplex in Breast Cancer Tumor Models.Chemical & biomedical imaging · 2026Article
- LINC01963 promotes pancreatic ductal adenocarcinoma proliferation via METTL3/IGF2BP2 axis-mediated m⁶A modification of c-Myc.Journal of experimental & clinical cancer research : CR · 2026Article
- Computational analysis of MYC gene variants: structural and functional impact of non-synonymous SNPs.Journal of applied genetics · 2026Article
- Lineage plasticity and histological transformation: tumor histology as a spectrum.Cell research · 2025Review
- Epithelial-Immune Cell Crosstalk in Salivary Gland Tumors: Implications for Tumor Progression and Diagnostic Assessment.International journal of molecular sciences · 2025Article
- Inverted chimeric RNAi molecules synergistically cotarget MYC and KRAS in KRAS-driven cancers.The Journal of clinical investigation · 2025Article
- MYC Point Mutations in Cancer: A Reboot and a Sequel.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Review
- MYC as a Target for Cancer Treatment: from Undruggable to Druggable?Targeted oncology · 2025Review
- Inhibition of tumor growth using A conjugated nanobody that specifically targets c-MYC.Oncogene · 2025Article
- Transcription Factors and Methods for the Pharmacological Correction of Their Activity.International journal of molecular sciences · 2025Review
- Myc family proteins: Molecular drivers of tumorigenesis and resistance in neuroendocrine tumors.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- Targeting SUMOylation in ovarian cancer: Sensitivity, resistance, and the role of MYC.iScience · 2025Article
- MYC in cancer: from undruggable target to clinical trials.Nature reviews. Drug discovery · 2025Review
- "Methyl jasmonate: bridging plant defense mechanisms and human therapeutics".Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
414 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Myc is a pleiotropic basic helix-loop-helix leucine zipper transcription factor that coordinates expression of the diverse intracellular and extracellular programs that together are necessary for growth and expansion of somatic cells. In principle, this makes inhibition of Myc an attractive pharmacological approach for treating diverse types of cancer. However, enthusiasm has been muted by lack of direct evidence that Myc inhibition would be therapeutically efficacious, concerns that it would induce serious side effects by inhibiting proliferation of normal tissues, and practical difficulties in designing Myc inhibitory drugs. We have modelled genetically both the therapeutic impact and the side effects of systemic Myc inhibition in a preclinical mouse model of Ras-induced lung adenocarcinoma by reversible, systemic expression of a dominant-interfering Myc mutant. We show that Myc inhibition triggers rapid regression of incipient and established lung tumours, defining an unexpected role for endogenous Myc function in the maintenance of Ras-dependent tumours in vivo. Systemic Myc inhibition also exerts profound effects on normal regenerating tissues. However, these effects are well tolerated over extended periods and rapidly and completely reversible. Our data demonstrate the feasibility of targeting Myc, a common downstream conduit for many oncogenic signals, as an effective, efficient and tumour-specific cancer therapy.
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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.