Evidence map›Paper›PMID 13678416›Full record

ReviewThe Biochemical journal2003

A perspective of polyamine metabolism.

Heather M Wallace, Alison V Fraser, Alun Hughes

Open access · bronzeAbstract readReview
In one paragraph

Review in The Biochemical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 297 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
297citing papers in PubMed, 1 pooled it
17.7field-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

297 citing papers in PubMed, 1 synthesis or guideline pooled it, 924 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Dietary polyamine intake and risk of colorectal adenomatous polyps.The American journal of clinical nutrition · 2012
    Trial
  5. iScience · 2026
    Article
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  9. Review
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  13. Bleomycin-induced lung fibrosis and dysfunction is exacerbated by G6PD deficiency.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
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237 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

3 authors at 1 institution in 1 country.

Heather M WallaceDepartment of Medicine and Therapeutics, University of Aberdeen, Polwarth Building, Foresterhill, Aberdeen AB25 2ZD, Scotland, UK. h.m.wallace@abdn.ac.uk
Alison V Fraser
Alun Hughes
University of Aberdeen · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polyamines are essential for the growth and function of normal cells. They interact with various macromolecules, both electrostatically and covalently and, as a consequence, have a variety of cellular effects. The complexity of polyamine metabolism and the multitude of compensatory mechanisms that are invoked to maintain polyamine homoeostasis argue that these amines are critical to cell survival. The regulation of polyamine content within cells occurs at several levels, including transcription and translation. In addition, novel features such as the +1 frameshift required for antizyme production and the rapid turnover of several of the enzymes involved in the pathway make the regulation of polyamine metabolism a fascinating subject. The link between polyamine content and human disease is unequivocal, and significant success has been obtained in the treatment of a number of parasitic infections. Targeting the polyamine pathway as a means of treating cancer has met with limited success, although the development of drugs such as DFMO (alpha-difluoromethylornithine), a rationally designed anticancer agent, has revolutionized our understanding of polyamine function in cell growth and provided 'proof of concept' that influencing polyamine metabolism and content within tumour cells will prevent tumour growth. The more recent development of the polyamine analogues has been pivotal in advancing our understanding of the necessity to deplete all three polyamines to induce apoptosis in tumour cells. The current thinking is that the polyamine inhibitors/analogues may also be useful agents in the chemoprevention of cancer and, in this area, we may yet see a revival of DFMO. The future will be in adopting a functional genomics approach to identifying polyamine-regulated genes linked to either carcinogenesis or apoptosis.

Indexed as

Antineoplastic AgentsBiological TransportCationsCell DeathCell DivisionEflornithineEnzyme InhibitorsModels, ChemicalPolyaminesAntineoplastic AgentsCationsEflornithineEnzyme InhibitorsPolyamines

Identifiers

PMID13678416
PMCPMC1223767
OpenAlexW1974620743

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.