ArticleProceedings of the National Academy of Sciences of the United States of America2003
A global transcriptional regulatory role for c-Myc in Burkitt's lymphoma cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 283 papers.
What it found
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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.
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Who cites it
283 citing papers in PubMed, 522 citations in OpenAlex.
- Trial
- MYC upregulation as candidate predictive biomarker for radioresistance in cervical cancer.Japanese journal of radiology · 2026Article
- Developmental timing distinguishes pediatric and adult cancers through retention and rewiring mechanisms.Nature communications · 2026Review
- Multi-Modal Deep Learning-Based Model to Predict Burkitt Lymphoma Recurrence.AMIA Joint Summits on Translational Science proceedings. AMIA Joint Summits on Translational Science · 2026Article
- Rewiring cancer metabolism: oncogenic signaling pathways and targeted therapeutics.Science China. Life sciences · 2025Review
- Pan-cancer Myc modulator that targets Myc-α-tubulin interaction to drive selective mitotic catastrophe.Scientific reports · 2025Article
- Reoviruses hijack the SMARCB1-MYC transcriptional regulation complex to activate autophagy for persistent viral infection in leafhopper vector.PLoS pathogens · 2025Article
- Potassium/sodium cation carriers robustly upregulate CD20 antigen by targeting MYC, and synergize with anti- CD20 immunotherapies to eliminate malignant B cells.Haematologica · 2025Article
- STK32C promotes colon tumor progression through activating c-MYC signaling.Cellular and molecular life sciences : CMLS · 2025Article
- GDP-mannose 4,6-dehydratase is a key driver of MYCN-amplified neuroblastoma core fucosylation and tumorigenesis.Oncogene · 2025Article
- PDCD11 Stabilizes C-MYC Oncoprotein by Hindering C-MYC-SKP2 Negative Feedback Loop to Facilitate Progression of p53-Mutant Breast and Colon Malignancies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Nuclear to Cytoplasmic Transport Is a Druggable Dependency in HDAC7-driven Small Cell Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Targeting protein synthesis pathways in MYC-amplified medulloblastoma.Discover oncology · 2025Review
- IL-7 promotes the formation of DNA double strand breaks and DNA repair in murine pro-B cells.Frontiers in immunology · 2025Article
- MYC overexpression in natural killer cell lymphoma: prognostic and therapeutic implications.Haematologica · 2024Article
- CRL2Oncogene · 2024Article
- MYC Oncogene: A Druggable Target for Treating Cancers with Natural Products.Aging and disease · 2024Review
- The DUX4-HIF1α Axis in Murine and Human Muscle Cells: A Link More Complex Than Expected.International journal of molecular sciences · 2024Article
- Approval of DFMO for high-risk neuroblastoma patients demonstrates a step of success to target MYC pathway.British journal of cancer · 2024Review
- Nuclear to cytoplasmic transport is a druggable dependency in MYC-driven hepatocellular carcinoma.Nature communications · 2024Article
223 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Overexpression of c-Myc is one of the most common alterations in human cancers, yet it is not clear how this transcription factor acts to promote malignant transformation. To understand the molecular targets of c-Myc function, we have used an unbiased genome-wide location-analysis approach to examine the genomic binding sites of c-Myc in Burkitt's lymphoma cells. We find that c-Myc together with its heterodimeric partner, Max, occupy >15% of gene promoters tested in these cancer cells. The DNA binding of c-Myc and Max correlates extensively with gene expression throughout the genome, a hallmark attribute of general transcription factors. The c-Myc/Max heterodimer complexes also colocalize with transcription factor IID in these cells, further supporting a general role for overexpressed c-Myc in global gene regulation. In addition, transcription of a majority of c-Myc target genes exhibits changes correlated with levels of c-myc mRNA in a diverse set of tissues and cell lines, supporting the conclusion that c-Myc regulates them. Taken together, these results suggest a general role for overexpressed c-Myc in global transcriptional regulation in some cancer cells and point toward molecular mechanisms for c-Myc function in malignant transformation.
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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.