Evidence map›Paper›PMID 23733953›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

MYC inhibition induces metabolic changes leading to accumulation of lipid droplets in tumor cells.

Hanna Zirath, Anna Frenzel, Ganna Oliynyk, Lova Segerström, Ulrica K Westermark, Karin Larsson, Matilda Munksgaard Persson, Kjell Hultenby, Janne Lehtiö, Christer Einvik and 4 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
163citing papers in PubMed, 1 pooled it
13.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

163 citing papers in PubMed, 1 synthesis or guideline pooled it, 237 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Targeting MYC-Driven Cancers: From Oncogenic Addiction to Therapeutic Vulnerability.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Combined targeting of PRDX6 and GSTP1 as a potential differentiation strategy for neuroblastoma treatment.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. CAMKIIδ Reinforces Lipid Metabolism and Promotes the Development of B Cell Lymphoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  18. Article
  19. Fueling the fire-a pan-cancer analysis of MYC-regulated lipid metabolism.Frontiers in cell and developmental biology · 2025
    Review
  20. Article

103 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 2 countries.

Hanna ZirathDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, SE-171 77 Stockholm, Sweden.
Anna Frenzel
Ganna Oliynyk
Lova Segerström
Ulrica K Westermark
Karin Larsson
Matilda Munksgaard Persson
Kjell Hultenby
Janne Lehtiö
Christer Einvik
Sven Påhlman
Per Kogner
Per-Johan Jakobsson
Marie Arsenian Henriksson
Karolinska Institutet · SELund University · SEScience for Life Laboratory · SEUniversity Hospital of North Norway · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The MYC genes are the most frequently activated oncogenes in human tumors and are hence attractive therapeutic targets. MYCN amplification leads to poor clinical outcome in childhood neuroblastoma, yet strategies to modulate the function of MYCN do not exist. Here we show that 10058-F4, a characterized c-MYC/Max inhibitor, also targets the MYCN/Max interaction, leading to cell cycle arrest, apoptosis, and neuronal differentiation in MYCN-amplified neuroblastoma cells and to increased survival of MYCN transgenic mice. We also report the discovery that inhibition of MYC is accompanied by accumulation of intracellular lipid droplets in tumor cells as a direct consequence of mitochondrial dysfunction. This study expands on the current knowledge of how MYC proteins control the metabolic reprogramming of cancer cells, especially highlighting lipid metabolism and the respiratory chain as important pathways involved in neuroblastoma pathogenesis. Together our data support direct MYC inhibition as a promising strategy for the treatment of MYC-driven tumors.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell DifferentiationCell Line, TumorCell ProliferationDisease Models, AnimalElectron TransportFatty AcidsHumansLipid MetabolismMiceMice, NudeMice, TransgenicMitochondriaNeuroblastoma5-(4-ethylbenzylidene)-2-thioxothiazolidin-4-oneAntineoplastic AgentsFatty AcidsProto-Oncogene Proteins c-mycReceptor, trkAThiazolescancer therapyfatty acid oxidationmitochondriaoxidative phosphorylationsmall molecule

Identifiers

PMID23733953
PMCPMC3690852
OpenAlexW2115141971

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.