Evidence map›Paper›PMID 36808622›Full record

ReviewThe EMBO journal2023

HIF: a master regulator of nutrient availability and metabolic cross-talk in the tumor microenvironment.

Rindert Missiaen, Nicholas P Lesner, M Celeste Simon

Open access · greenAbstract readReview
In one paragraph

Review in The EMBO journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
12.4field-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

41 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
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  8. Ipriflavone FromMedComm · 2026
    Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Introduction to Cancer Metabolism.Cancer treatment and research · 2026
    Review
  15. The role and mechanisms of the HIF-1 signaling pathway in LC-COPD.Journal of cancer research and clinical oncology · 2025
    Review
  16. Making sense of oxygen sensing.The EMBO journal · 2025
    Article
  17. Review
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Rindert MissiaenAbramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Nicholas P LesnerAbramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
M Celeste SimonAbramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.ORCID 0000-0001-9106-447X
Cancer Research Institute · US

Funding

TRANSLATIONAL CONTROL IN ADAPTATION TO HYPOXIAP01CA104838 · NCI · UNIVERSITY OF PENNSYLVANIA · PI KEITH, BRIAN · 2004 to 2018
$17.6M
IMMUNOBIOLOGY OF NORMAL AND NEOPLASTIC LYMPHOCYTEST32CA009140 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Malay Haldar, WARREN S PEAR · 1985 to 2026
$16.1M
Metabolic Tumor Suppressors in Renal Cancer: Unprecedented Roles in Disease ProgressionR35CA220483 · NCI · UNIVERSITY OF PENNSYLVANIA · PI M. CELESTE SIMON · 2017 to 2026
$9.4M
NCI NIH HHS P01 CA104838NCI NIH HHS R35 CA220483NCI NIH HHS T32 CA009140
6 · The paper itself

Abstract

A role for hypoxia-inducible factors (HIFs) in hypoxia-dependent regulation of tumor cell metabolism has been thoroughly investigated and covered in reviews. However, there is limited information available regarding HIF-dependent regulation of nutrient fates in tumor and stromal cells. Tumor and stromal cells may generate nutrients necessary for function (metabolic symbiosis) or deplete nutrients resulting in possible competition between tumor cells and immune cells, a result of altered nutrient fates. HIF and nutrients in the tumor microenvironment (TME) affect stromal and immune cell metabolism in addition to intrinsic tumor cell metabolism. HIF-dependent metabolic regulation will inevitably result in the accumulation or depletion of essential metabolites in the TME. In response, various cell types in the TME will respond to these hypoxia-dependent alterations by activating HIF-dependent transcription to alter nutrient import, export, and utilization. In recent years, the concept of metabolic competition has been proposed for critical substrates, including glucose, lactate, glutamine, arginine, and tryptophan. In this review, we discuss how HIF-mediated mechanisms control nutrient sensing and availability in the TME, the competition for nutrients, and the metabolic cross-talk between tumor and stromal cells.

Indexed as

NeoplasmsTumor MicroenvironmentCell HypoxiaHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitNutrientsHypoxia-Inducible Factor 1, alpha SubunitNutrientsHIFtumor metabolismtumor microenvironment

Identifiers

PMID36808622
PMCPMC10015374
OpenAlexW4321373217

What Socratic 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 Socratic graph.