ArticleOncogene2015
A common functional consequence of tumor-derived mutations within c-MYC.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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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
21 citing papers in PubMed, 36 citations in OpenAlex.
- MYC Point Mutations in Cancer: A Reboot and a Sequel.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Review
- Article
- MYC promotes global transcription in part by controlling P-TEFb complex formation via DNA-binding independent inhibition of CDK9 SUMOylation.Science China. Life sciences · 2023Article
- Network-based assessment of HDAC6 activity predicts preclinical and clinical responses to the HDAC6 inhibitor ricolinostat in breast cancer.Nature cancer · 2023Article
- Splice-switch oligonucleotide-based combinatorial platform prioritizes synthetic lethal targets CHK1 and BRD4 against MYC-driven hepatocellular carcinoma.Bioengineering & translational medicine · 2023Article
- Spotlight on New Therapeutic Opportunities for MYC-Driven Cancers.OncoTargets and therapy · 2023Review
- Targeting Transcription Factors in Cancer: From "Undruggable" to "Druggable".Methods in molecular biology (Clifton, N.J.) · 2023Article
- T-cell Dysfunction upon Expression of MYC with Altered Phosphorylation at Threonine 58 and Serine 62.Molecular cancer research : MCR · 2022Article
- The MYC oncoprotein directly interacts with its chromatin cofactor PNUTS to recruit PP1 phosphatase.Nucleic acids research · 2022Article
- Review
- Two diphosphorylated degrons control c-Myc degradation by the Fbw7 tumor suppressor.Science advances · 2022Article
- Article
- Distinct genetic changes reveal evolutionary history and heterogeneous molecular grade of DLBCL with MYC/BCL2 double-hit.Leukemia · 2020Article
- MYC dephosphorylation by the PP1/PNUTS phosphatase complex regulates chromatin binding and protein stability.Nature communications · 2018Article
- SIRT1 regulates Mxd1 during malignant melanoma progression.Oncotarget · 2017Article
- Lysine-52 stabilizes the MYC oncoprotein through an SCFOncogene · 2017Article
- MYC Deregulation in Primary Human Cancers.Genes · 2017Review
- MYC-nick promotes cell migration by inducing fascin expression and Cdc42 activation.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Clinical and Biologic Significance of MYC Genetic Mutations in De Novo Diffuse Large B-cell Lymphoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Glucose induced activation of canonical Wnt signaling pathway in hepatocellular carcinoma is regulated by DKK4.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
The relevance of changes to the coding sequence of the c-MYC oncogene to malignancy is controversial. Overexpression of a pristine form of MYC is observed in many cancers and is sufficient to drive tumorigenesis in most contexts. Yet missense changes to MYC are found in ~50% of Burkitt's lymphomas, aggregate within an amino-terminal degron important for proteasomal destruction of MYC, and where examined profoundly enhance the tumorigenic properties of MYC in vitro and in vivo. Much of the controversy surrounding these mutants stems from the limited number of mutations that have been evaluated and their clustering within a single region of the MYC protein; the highly-conserved Myc box I (MbI) element. Here, by analysis of extant genomic data sets, we identify a previously unrecognized hotspot for tumor-associated MYC mutations, located in a conserved central portion of the protein. We show that, despite their distal location in MYC, mutations in this region precisely phenocopy those in MbI in terms of stability, in vitro transformation, growth-promoting properties, in vivo tumorigenesis and ability to escape p53-dependent tumor surveillance mechanisms. The striking parallels between the behavior of tumor-derived mutations in disparate regions of the MYC protein reveals that a common molecular process is disrupted by these mutations, implying an active role for these mutations in tumorigenesis and suggesting that different therapeutic strategies may be needed for treatment of lymphomas expressing wild type versus mutant forms of MYC protein.
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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.