Evidence map›Paper›PMID 36696004›Full record

ReviewCancer metastasis reviews2023

The role of cancer cell bioenergetics in dormancy and drug resistance.

Steven Tau, Todd W Miller

Open access · greenAbstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

12 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. EGFR-TKIs Induced DPP4 Drives Metabolic Reprogramming of Persister Cells in Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  7. Article
  8. Review
  9. Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  10. Article
  11. Review
  12. Review
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

2 authors at 1 institution in 1 country.

Steven TauDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Dartmouth Cancer Center, Lebanon, NH, USA.
Todd W MillerDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Dartmouth Cancer Center, Lebanon, NH, USA. Todd.W.Miller@dartmouth.edu.ORCID http://orcid.org/0000-0001-8912-2909
Dartmouth College · US

Funding

Translational Engineering in Cancer (TEC)P30CA023108 · NCI · DARTMOUTH COLLEGE · PI Fred W Kolling IV · 1985 to 2026
$91.3M
A precision medicine basis for estrogen therapy for advanced breast cancerR01CA200994 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI Todd W. Miller · 2017 to 2026
$3.7M
Therapeutically leveraging metabolic vulnerabilities in breast cancerR01CA262232 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI Todd W. Miller · 2022 to 2026
$2.2M
Timing is everything: applications in precision oncology for ER+ breast cancerR01CA211869 · NCI · DARTMOUTH COLLEGE · PI MILLER, TODD W. · 2017 to 2021
$2.1M
Uncovering the basis and implications of lineage plasticity in breast cancerR01CA267691 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI Todd W. Miller · 2022 to 2026
$1.8M
NCI NIH HHS P30 CA023108NCI NIH HHS P30CA023108NCI NIH HHS R01 CA200994NCI NIH HHS R01CA200994NCI NIH HHS R01 CA211869NCI NIH HHS R01CA211869NCI NIH HHS R01 CA262232NCI NIH HHS R01CA262232NCI NIH HHS R01 CA267691NCI NIH HHS R01CA267691
6 · The paper itself

Abstract

While anti-cancer drug treatments are often effective for the clinical management of cancer, these treatments frequently leave behind drug-tolerant persister cancer cells that can ultimately give rise to recurrent disease. Such persistent cancer cells can lie dormant for extended periods of time, going undetected by conventional clinical means. Understanding the mechanisms that such dormant cancer cells use to survive, and the mechanisms that drive emergence from dormancy, is critical to the development of improved therapeutic strategies to prevent and manage disease recurrence. Cancer cells often exhibit metabolic alterations compared to their non-transformed counterparts. An emerging body of evidence supports the notion that dormant cancer cells also have unique metabolic adaptations that may offer therapeutically targetable vulnerabilities. Herein, we review mechanisms through which cancer cells metabolically adapt to persist during drug treatments and develop drug resistance. We also highlight emerging therapeutic strategies to target dormant cancer cells via their metabolic features.

Indexed as

Antineoplastic AgentsNeoplasmsDrug Resistance, NeoplasmEnergy MetabolismHumansAntineoplastic AgentsCancerEnergyFatty acidGlucoseMetabolismTumor

Identifiers

PMID36696004
PMCPMC10233409
OpenAlexW4317932659

What OpenQuestion holds

Textmetadata
LicenceTDM
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.