Evidence map›Paper›PMID 24280044›Full record

ArticleCancer & metabolism2013

Activated lymphocytes as a metabolic model for carcinogenesis.

Andrew N Macintyre, Jeffrey C Rathmell

Open access · goldAbstract read
In one paragraph

Article in Cancer & metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

53 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Asparagine restriction enhances CD8Nature metabolism · 2023
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Inside-Out of Complement in Cancer.Frontiers in immunology · 2022
    Review
  13. Redox regulation of immunometabolism.Nature reviews. Immunology · 2021
    Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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.

Andrew N MacintyreDepartment of Pharmacology and Cancer Biology, Department of Immunology, Sarah W, Stedman Nutrition and Metabolism Center, Duke University, Durham, NC, 27710, USA. jeff.rathmell@duke.edu.
Jeffrey C Rathmell
Duke University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic reprogramming is a key event in tumorigenesis to support cell growth, and cancer cells frequently become both highly glycolytic and glutamine dependent. Similarly, T lymphocytes (T cells) modify their metabolism after activation by foreign antigens to shift from an energetically efficient oxidative metabolism to a highly glycolytic and glutamine-dependent metabolic program. This metabolic transition enables T cell growth, proliferation, and differentiation. In both activated T cells and cancer cells metabolic reprogramming is achieved by similar mechanisms and offers similar survival and cell growth advantages. Activated T cells thus present a useful model with which to study the development of tumor metabolism. Here, we review the metabolic similarities and distinctions between activated T cells and cancer cells, and discuss both the common signaling pathways and master metabolic regulators that lead to metabolic rewiring. Ultimately, understanding how and why T cells adopt a cancer cell-like metabolic profile may identify new therapeutic strategies to selectively target tumor metabolism or inflammatory immune responses.

Identifiers

PMID24280044
PMCPMC3834493
OpenAlexW2145682243

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.