ArticleCancer biology & therapy2022
Target c-Myc to treat pancreatic cancer.
Article in Cancer biology & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed.
- Synthetic lethality targets in pancreatic ductal adenocarcinoma: prevalence and limitations of liquid biopsy detection in a minority-serving cancer center.Future oncology (London, England) · 2026Article
- Carbohydrates metabolic reprogramming and tumor microenvironment in pancreatic cancer: targeting pathways.Molecular biology reports · 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
- Pancreatic ductal adenocarcinoma: integrating molecular insights for targeted interventions.Signal transduction and targeted therapy · 2026Review
- Rationally and in silico guided APOBEC3F-directed CBE for enhanced PDAC genetic therapy.Communications biology · 2026Article
- Evidence that extra copies of chromosome 1q play a role in the early phases of pancreatic neoplasia.Science advances · 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
- Combined HDAC and eIF4A inhibition: A novel epigenetic therapy for pancreatic ductal adenocarcinoma.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2026Article
- Plexin Domain Containing 2, a Protein Specifically Expressed and Elevated in Human Pancreatic Cancer Tissue and Serum, Influences Cell Proliferation by Correlating With Cortactin.Cancer medicine · 2025Article
- α-hederin decreases the glycolysis level in intestinal epithelial cells via SNX10-mediated DEPDC5 degradation.Journal of pharmaceutical analysis · 2025Article
- LTBP2 promotes meningioma progression by enhancing glycolysis via the PI3K/AKT/mTOR/c-Myc signaling pathway.Discover oncology · 2025Article
- PEITC restores chemosensitivity in cisplatin-resistant non-small cell lung cancer by targeting c-Myc/miR-424-5p.Discover oncology · 2025Article
- Network pharmacology and experimental study on the inhibition of glycolysis by amentoflavone in pancreatic cancer.Discover oncology · 2025Article
- SLB-msSIM: A Spectral Library-Based Multiplex Segmented SIM Platform for Single-Cell Proteomic Analysis.Proteomics · 2025Article
- Beyond the tumor: Enhancing pancreatic cancer therapy through glutamine metabolism and innovative drug delivery.Journal of cell communication and signaling · 2025Review
- CX26 promotes pancreatic cancer progression by competitively inhibiting interaction of c-Myc with PSMD2 and enhancing c-Myc stability.Journal of translational medicine · 2025Article
- TFAP2A enhances tumor stemness and promotes metastasis in pancreatic ductal adenocarcinoma.iScience · 2025Article
- Multifaceted Cooperation Between WNT and PI3K Signaling Axis through the Long Noncoding RNA SNHG16 and TCF7 in de novo Acute Lymphoblastic Leukemia Patients.Iranian biomedical journal · 2025Article
- Deciphering of SOX9 Functions in Pancreatic Cancer Cells.International journal of molecular sciences · 2025Article
- Molecular principles underlying aggressive cancers.Signal transduction and targeted therapy · 2025Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C-Myc overexpression is a common finding in pancreatic cancer and predicts the aggressive behavior of cancer cells. It binds to the promoter of different genes, thereby regulating their transcription. C-Myc is downstream of KRAS and interacts with several oncogenic and proliferative pathways in pancreatic cancer. C-Myc enhances aerobic glycolysis in cancer cells and regulates glutamate biosynthesis from glutamine. It provides enough energy for cancer cells' metabolism and sufficient substrate for the synthesis of organic molecules. C-Myc overexpression is associated with chemoresistance, intra-tumor angiogenesis, epithelial-mesenchymal transition (EMT), and metastasis in pancreatic cancer. Despite its title, c-Myc is not "undruggable" and recent studies unveiled that it can be targeted, directly or indirectly. Small molecules that accelerate c-Myc ubiquitination and degradation have been effective in preclinical studies. Small molecules that hinder c-Myc-MAX heterodimerization or c-Myc/MAX/DNA complex formation can functionally inhibit c-Myc. In addition, c-Myc can be targeted through transcriptional, post-transcriptional, and translational modifications.
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