ArticleCancer research2008
Genomic and proteomic analysis reveals a threshold level of MYC required for tumor maintenance.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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Who cites it
56 citing papers in PubMed, 90 citations in OpenAlex.
- Article
- A tumorigenesis threshold for endogenous Myc revealed by dosage-compensation for Myc-haploinsufficiency in the absence of p53.bioRxiv : the preprint server for biology · 2025Article
- MYC function and regulation in physiological perspective.Frontiers in cell and developmental biology · 2023Review
- Review
- The MYC oncogene - the grand orchestrator of cancer growth and immune evasion.Nature reviews. Clinical oncology · 2022Review
- Luminescence complementation technology for the identification of MYC:TRRAP inhibitors.Oncotarget · 2021Article
- Targeted Downregulation of MYC through G-quadruplex Stabilization by DNAi.Molecules (Basel, Switzerland) · 2021Article
- A mathematical model of tumor regression and recurrence after therapeutic oncogene inactivation.Scientific reports · 2021Article
- Targeting the MYC Ubiquitination-Proteasome Degradation Pathway for Cancer Therapy.Frontiers in oncology · 2021Review
- Methods of Expression, Purification, and Preparation of the c-Myc b-HLH-LZ for Its Biophysical Characterization.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Hallmarks of cancer-the new testament.Open biology · 2021Review
- c-Myc inactivation of p53 through the pan-cancer lncRNA MILIP drives cancer pathogenesis.Nature communications · 2020Article
- Evidence for immortality and autonomy in animal cancer models is often not provided, which causes confusion on key issues of cancer biology.Journal of Cancer · 2020Review
- Formation of a structurally-stable conformation by the intrinsically disordered MYC:TRRAP complex.PloS one · 2019Article
- Site-specific amino acid substitution in dodecameric peptides determines the stability and unfolding of c-MYC quadruplex promoting apoptosis in cancer cells.Nucleic acids research · 2018Article
- The MYC transcription factor network: balancing metabolism, proliferation and oncogenesis.Frontiers of medicine · 2018Review
- Article
- Article
- Article
- DNMT3B overexpression contributes to aberrant DNA methylation and MYC-driven tumor maintenance in T-ALL and Burkitt's lymphoma.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
MYC overexpression has been implicated in the pathogenesis of most types of human cancers. MYC is likely to contribute to tumorigenesis by its effects on global gene expression. Previously, we have shown that the loss of MYC overexpression is sufficient to reverse tumorigenesis. Here, we show that there is a precise threshold level of MYC expression required for maintaining the tumor phenotype, whereupon there is a switch from a gene expression program of proliferation to a state of proliferative arrest and apoptosis. Oligonucleotide microarray analysis and quantitative PCR were used to identify changes in expression in 3,921 genes, of which 2,348 were down-regulated and 1,573 were up-regulated. Critical changes in gene expression occurred at or near the MYC threshold, including genes implicated in the regulation of the G(1)-S and G(2)-M cell cycle checkpoints and death receptor/apoptosis signaling. Using two-dimensional protein analysis followed by mass spectrometry, phospho-flow fluorescence-activated cell sorting, and antibody arrays, we also identified changes at the protein level that contributed to MYC-dependent tumor regression. Proteins involved in mRNA translation decreased below threshold levels of MYC. Thus, at the MYC threshold, there is a loss of its ability to maintain tumorigenesis, with associated shifts in gene and protein expression that reestablish cell cycle checkpoints, halt protein translation, and promote apoptosis.
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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.