Cited by 3,390Cancer-related Molecular PathwaysPI3K/AKT/mTOR signaling in cancerCancer, Hypoxia, and Metabolism

MYC on the Path to Cancer

Open access
Dang, Chi V.·2012·Cell

Abstract

The MYC oncogene contributes to the genesis of many human cancers. Recent insights into its expression and function have led to therapeutic opportunities. MYC's activation by bromodomain proteins could be inhibited by drug-like molecules, resulting in tumor inhibition in vivo. Tumor growth can also be curbed by pharmacologically uncoupling bioenergetic pathways involving glucose or glutamine metabolism from Myc-induced cellular biomass accumulation. Other approaches to halt Myc on the path to cancer involve targeting Myc-Max dimerization or Myc-induced microRNA expression. Here the richness of our understanding of MYC is reviewed, highlighting new biological insights and opportunities for cancer therapies.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.cell.2012.03.003

Cites

232 of 232 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The Myc oncogene, including its three subtypes C-Myc, N-Myc, and L-Myc, is believed to act as a transcriptional "amplifier" that can trigger a variety of oncogenic transcriptional programs in different types of cancer.

    “The Myc oncogene, including its three subtypes C-Myc, N-Myc, and L-Myc, is believed to act as a transcriptional “amplifier” that can trigger a variety of oncogenic transcriptional programs in different types of cancer.410,411”
  • Overexpression or hyperactivation of Myc is one of the most common occurrences in cancer, making it a key factor in oncogenesis.

    “Overexpression or hyperactivation of Myc is one of the most common occurrences in cancer, making it a key factor in oncogenesis.”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Dang, C. V.
Affiliations
Abramson Cancer Center (US)
Corresponding author
Dang, Chi V.
Venue
Cell
Publisher
Elsevier BV
Published
2012-03
Volume
149
Issue
1
Pages
22-35
ISSN
0092-8674 (ISSN-L)
OpenAlex
W2021536610
Cited by
3,390
References
232
Citations by year
2026: 218 · 2025: 267 · 2024: 300 · 2023: 299 · 2022: 280 · 2021: 332 · 2020: 283 · 2019: 250 · 2018: 209 · 2017: 215 · 2016: 215 · 2015: 166 · 2014: 179 · 2013: 144 · 2012: 33
FWCI
17.26
Type
journal article
Language
en
Open access
Locations
  • Cell (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Cancer Institute (R01CA057341, R01CA051497, P30CA016520)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Keywords
MYC oncogene, tumor initiation, bromodomain proteins, MYC inhibitors, tumor growth inhibition, bioenergetics, glucose metabolism, glutamine metabolism, biomass accumulation, microRNA expression, cancer therapy
MeSH terms
Animals, Cell Transformation, Neoplastic, Humans, Neoplasms, Gene Expression Regulation, Neoplastic, Genes, myc, Proto-Oncogene Proteins c-myc, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review