Evidence map›Paper›PMID 22737668›Full record

ArticleFrontiers in oncology2012

The proline regulatory axis and cancer.

James Ming Phang, Wei Liu, Chad Hancock, Kyle J Christian

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

97 citing papers in PubMed, 161 citations in OpenAlex.

  1. Article
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  11. Review
  12. Targeting the glutamine-arginine-proline metabolism axis in cancer.Journal of enzyme inhibition and medicinal chemistry · 2024
    Review
  13. Article
  14. Article
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  17. Article
  18. Review
  19. Article
  20. Caffeic Acid and Diseases-Mechanisms of Action.International journal of molecular sciences · 2022
    Review

37 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

4 authors at 2 institutions in 3 countries.

James Ming PhangMetabolism and Cancer Susceptibility Section, Basic Research Laboratory, Center for Cancer Research, Frederick National Laboratory for Cancer Research Frederick, MD, USA.
Wei Liu
Chad Hancock
Kyle J Christian
Center for Cancer Research · USInserm · FR

Funding

Metabolic Mechanisms for Programmed Cell DeathZIABC010743 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI PHANG, JAMES M · 2009 to 2015
$3.1M
Regulation of Proline Oxidase for Bioenergetics during Nutrient StressZIABC010744 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI PHANG, JAMES M · 2009 to 2015
$2.3M
Extracellular Matrix and Stress Substrates: the Role of ProlidaseZIABC010746 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI PHANG, JAMES M · 2009 to 2015
$1.0M
6 · The paper itself

Abstract

Studies in metabolism and cancer have characterized changes in core pathways involving glucose and glutamine, emphasizing the provision of substrates for building cell mass. But recent findings suggest that pathways previously considered peripheral may play a critical role providing mechanisms for cell regulation. Several of these mechanisms involve the metabolism of non-essential amino acids, for example, the channeling of glycolytic intermediates into the serine pathway for one-carbon transfers. Historically, we proposed that the proline biosynthetic pathway participated in a metabolic interlock with glucose metabolism. The discovery that proline degradation is activated by p53 directed our attention to the initiation of apoptosis by proline oxidase/dehydrogenase. Now, however, we find that the biosynthetic mechanisms and the metabolic interlock may depend on the pathway from glutamine to proline, and it is markedly activated by the oncogene MYC. These findings add a new dimension to the proline regulatory axis in cancer and present attractive potential targets for cancer treatment.

Indexed as

glutamine metabolismMYC oncogeneproline metabolismredox regulationtumor suppressor function

Identifiers

PMID22737668
PMCPMC3380417
OpenAlexW2103304356

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.