ReviewSignal transduction and targeted therapy2024
MYC and KRAS cooperation: from historical challenges to therapeutic opportunities in cancer.
Review in Signal transduction and targeted therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed.
- Surufatinib plus tislelizumab as later-line therapy for metastatic colorectal cancer: a single-arm, phase II trial.BMC cancer · 2026Trial
- Transcriptomic Profiling of Canine Mammary Tumours Reveals Significant Heterogeneity Between and Within Histological Classes.Veterinary and comparative oncology · 2026Article
- Daraxonrasib and Beyond: Pan-RAS Inhibition, Resistance, and Next-Generation Strategies.Cancer science · 2026Review
- Developmental timing distinguishes pediatric and adult cancers through retention and rewiring mechanisms.Nature communications · 2026Review
- Targeting the Undruggable: Deep Learning-Driven Design of Peptide Therapeutics in Cancer.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Efficacy and immunogenic effects of Tumor Treating Fields (TTFields) in preclinical models of pancreatic ductal adenocarcinoma, with and without gemcitabine/nab-paclitaxel.International journal of cancer · 2026Article
- p27 Expression in Wild-Type KRAS Colon Cancer.Journal of cellular and molecular medicine · 2026Article
- c-MYC is Transcribed in a Circadian Manner and Acts a Clock Disruptor whose Timing Minimizes its Impacts.bioRxiv : the preprint server for biology · 2026Article
- Optimizing the Efficacy-Toxicity Paradigm in Pediatric Oncology: A Narrative Review of Immunotherapy and Survivorship Outcomes.Current oncology (Toronto, Ont.) · 2026Review
- Pancreatic ductal adenocarcinoma: integrating molecular insights for targeted interventions.Signal transduction and targeted therapy · 2026Review
- Pancancer Fine-Mapping of Mutational Intolerance Identifies CHEK1 as an Immunosuppressive Driver in Lung Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Dual Role of LBH589 in Triple-Negative Breast Cancer: Inhibition of Tumor Growth and Enhancement of Antitumor Immunity.Cancer reports (Hoboken, N.J.) · 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
- Evolution and Functional Implications of Codon Usage Bias in Eukaryotes.Journal of molecular evolution · 2026Review
- The Art of Domesticating Proteins: How Cancer Cells Adapt to Therapeutic and Environmental Stressors.International journal of molecular sciences · 2026Review
- Rationally and in silico guided APOBEC3F-directed CBE for enhanced PDAC genetic therapy.Communications biology · 2026Article
- Molecular Mechanisms of Juvenile Nasopharyngeal Angiofibroma: A Narrative Review.Current oncology (Toronto, Ont.) · 2026Review
- Article
- Epigenetic modulation to overcome immune suppression in pancreatic cancer.Clinical epigenetics · 2026Review
- Genetic landscape of cancer: mechanisms, key genes, and therapeutic implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
RAS and MYC rank amongst the most commonly altered oncogenes in cancer, with RAS being the most frequently mutated and MYC the most amplified. The cooperative interplay between RAS and MYC constitutes a complex and multifaceted phenomenon, profoundly influencing tumor development. Together and individually, these two oncogenes regulate most, if not all, hallmarks of cancer, including cell death escape, replicative immortality, tumor-associated angiogenesis, cell invasion and metastasis, metabolic adaptation, and immune evasion. Due to their frequent alteration and role in tumorigenesis, MYC and RAS emerge as highly appealing targets in cancer therapy. However, due to their complex nature, both oncogenes have been long considered "undruggable" and, until recently, no drugs directly targeting them had reached the clinic. This review aims to shed light on their complex partnership, with special attention to their active collaboration in fostering an immunosuppressive milieu and driving immunotherapeutic resistance in cancer. Within this review, we also present an update on the different inhibitors targeting RAS and MYC currently undergoing clinical trials, along with their clinical outcomes and the different combination strategies being explored to overcome drug resistance. This recent clinical development suggests a paradigm shift in the long-standing belief of RAS and MYC "undruggability", hinting at a new era in their therapeutic targeting.
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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.