Evidence map›Paper›PMID 19072739›Full record

ReviewMolecular nutrition & food research2009

From delocalized lipophilic cations to hypoxia: blocking tumor cell mitochondrial function leads to therapeutic gain with glycolytic inhibitors.

Metin Kurtoglu, Theodore J Lampidis

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Molecular nutrition & food research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06566443 (Phase I Trial Evaluating the Safety of the Dietary Supplement Honokiol in Early-Stage Resectable Non-Small Cell Lung Cancer), which is not on this map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.4field-weighted citation impact, top 21% 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.

NCT06566443 phase1recruitingnot on this mapstarted 2025, after this paper: background citation

Phase I Trial Evaluating the Safety of the Dietary Supplement Honokiol in Early-Stage Resectable Non-Small Cell Lung Cancer

TypeinterventionalSponsorThe Methodist Hospital Research InstituteRan2025 to 2027Enrolled15ConditionsCarcinoma, Non-Small-Cell LungArmsHonokiol
3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. CytochromeExperimental and therapeutic medicine · 2016
    Article
  14. Article
  15. Dual-targeting of aberrant glucose metabolism in glioblastoma.Journal of experimental & clinical cancer research : CR · 2015
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Tunable cytotoxicity of rhodamine 6G via anion variations.Journal of the American Chemical Society · 2013
    Article
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 2 institutions in 2 countries.

Metin KurtogluMiller School of Medicine, University of Miami, Miami, FL 33136, USA.
Theodore J Lampidis
Institute of Cell Biology and Neurobiology · ITUniversity of Miami · US

Funding

Role of Mitochondria and Glycolysis in Tumor Cell MDRR01CA037109 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI LAMPIDIS, THEODORE J · 1985 to 2011
$3.3M
NCI NIH HHS R01 CA037109
6 · The paper itself

Abstract

An unexpected similarity between cancer and cardiac muscle cells in their sensitivity to anthracyclines and delocalized lipophilic cations (DLC) prompted a series of studies in which it was shown that the positive charge of these compounds is central to their selective accumulation and toxicity in these two distinct cell types. An initial finding to explain this phenomenon was that cancer and cardiac muscle cells exhibit high negative plasma membrane potentials resulting in increased uptake of these agents. However, the p-glycoprotein efflux pump was shown to be another factor underlying differential accumulation of these compounds, since it recognizes positively charged drugs and thereby actively reduces their intracellular concentrations. The delocalized positive charge and lipophilicity of DLCs leads to their retention and inhibition of ATP synthesis in mitochondria. Years later it was realized that cancer cells in the hypoxic portions of solid tumors were similar to those treated with DLCs in relying mainly on anaerobic metabolism for survival and could thus be targeted with a glycolytic inhibitor, 2-deoxy-D-glucose (2-DG). This hypothesis has lead to a Phase I clinical trial in which 2-DG is used to selectively kill the hypoxic tumor cell population which are resistant to standard chemotherapy or radiation.

Indexed as

AnthracyclinesAntineoplastic AgentsCationsCell HypoxiaDeoxyglucoseGlycolysisHumansHypoxiaMitochondriaNeoplasmsReference ValuesRhodamine 123AnthracyclinesAntineoplastic AgentsCationsDeoxyglucoseRhodamine 123

Identifiers

PMID19072739
PMCPMC2928140
OpenAlexW1969704731

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.