ReviewThe EMBO journal2017
MYC and tumor metabolism: chicken and egg.
Review in The EMBO journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 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
146 citing papers in PubMed, 249 citations in OpenAlex.
- Monocyte Dll4 Contributes to Systemic Inflammation in People Living With HIV.Circulation research · 2026Article
- NNMT Loss Drives Cancer Progression by enhancing SAM availability for mTORC1 Signaling and Chromatin Methylation.bioRxiv : the preprint server for biology · 2026Article
- MTHFR functions as a metabolic checkpoint in NSCLC through SLC25A26-mediated SHMT2 inhibition.Cell death & disease · 2026Article
- Oncogene c‑Myc: From molecular mechanism to targeted therapy (Review).Molecular medicine reports · 2026Review
- Oncogenic DCTPP1/MYC feedback loop rewires pyrimidine metabolism to drive hepatocellular carcinoma.Functional & integrative genomics · 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
- Nucleolus as a cornerstone linking proliferation and metabolism to cellular responses to stress: involvement of transcription factors MYC and p53.Frontiers in molecular biosciences · 2026Review
- Targeting aerobic glycolysis by quercetin inhibits acute monocytic leukemia SHI-1 cells.Annals of medicine and surgery (2012) · 2025Article
- c-Myc Inhibits Macrophage Antimycobacterial Response in Mycobacterium tuberculosis Infection.The Journal of infectious diseases · 2025Article
- VRK2 targeting potentiates anti-PD-1 immunotherapy in hepatocellular carcinoma through MYC destabilization.Nature communications · 2025Article
- Lysosome-dependent nutrient scavenging underlies stress adaptation during epithelial-to-mesenchymal transition.bioRxiv : the preprint server for biology · 2025Article
- MYC as a Target for Cancer Treatment: from Undruggable to Druggable?Targeted oncology · 2025Review
- Polydatin: A natural compound with multifaceted anticancer properties.Journal of traditional and complementary medicine · 2025Review
- Pyruvate kinase M2 modulates Japanese encephalitis virus replication in neuronal cells.The Journal of general virology · 2025Article
- PRPS activity tunes redox homeostasis in Myc-driven lymphoma.Redox biology · 2025Article
- c-Myc inhibits macrophage antimycobacterial response inbioRxiv : the preprint server for biology · 2025Article
- Effect of deubiquitinases in head and neck squamous cell carcinoma (Review).Oncology letters · 2025Review
- Computational modeling of cancer cell metabolism along the catabolic-anabolic axes.NPJ systems biology and applications · 2025Article
- Exploring the metabolic alterations in cervical cancer induced by HPV oncoproteins: From mechanisms to therapeutic targets.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- The Role of Non-Coding RNAs in MYC-Mediated Metabolic Regulation: Feedback Loops and Interactions.Non-coding RNA · 2025Review
86 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcription factors of the MYC family are deregulated in the majority of all human cancers. Oncogenic levels of MYC reprogram cellular metabolism, a hallmark of cancer development, to sustain the high rate of proliferation of cancer cells. Conversely, cells need to modulate MYC function according to the availability of nutrients, in order to avoid a metabolic collapse. Here, we review recent evidence that the multiple interactions of MYC with cell metabolism are mutual and review mechanisms that control MYC levels and function in response to metabolic stress situations. The main hypothesis we put forward is that regulation of MYC levels is an integral part of the adaptation of cells to nutrient deprivation. Since such mechanisms would be particularly relevant in tumor cells, we propose that-in contrast to growth factor-dependent controls-they are not disrupted during tumorigenesis and that maintaining flexibility of expression is integral to MYC's oncogenic function.
Indexed as
Identifiers
What OpenQuestion holds
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.