Evidence map›Paper›PMID 31406492›Full record

ArticleCurrent colorectal cancer reports2018

Colorectal Cancer and Metabolism.

Rachel E Brown, Sarah P Short, Christopher S Williams

Abstract read
In one paragraph

Article in Current colorectal cancer reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
6.3field-weighted citation impact, top 2% 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

76 citing papers in PubMed, 138 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Metabolic stress conditions dictate MAPKAPK2-dependent efficiency of MEK1/2 inhibition in colorectal carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Article
  7. The emerging metabolic role and treatment target of CPT1A in CRC.Frontiers in cell and developmental biology · 2026
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
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  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

16 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 2 institutions in 1 country.

Rachel E BrownProgram in Cancer Biology, Vanderbilt University, Nashville, TN, USA.
Sarah P ShortProgram in Cancer Biology, Vanderbilt University, Nashville, TN, USA.
Christopher S WilliamsProgram in Cancer Biology, Vanderbilt University, Nashville, TN, USA.
Vanderbilt University · USVanderbilt University Medical Center · US

Funding

Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007347 · NIGMS · VANDERBILT UNIVERSITY · PI WILLIAMS, CHRISTOPHER S. · 1985 to 2023
$26.3M
Selenium in gastrointestinal inflammatory diseasesR01DK099204 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WILLIAMS, CHRISTOPHER S. · 2014 to 2018
$1.8M
Tissue-specific contribution of Selenoprotein P in colitis and oxidative damageF32DK108492 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI SHORT, SARAH PALMER · 2016 to 2018
$170k
Mechanisms of Transcriptional Regulation by MTG16 in the IntestineF30DK120149 · NIDDK · VANDERBILT UNIVERSITY · PI BROWN, RACHEL ELIZABETH · 2018 to 2021
$146k
Modulation of Junctional Signaling by BVES in Colorectal CarcinomaI01BX001426 · VA · VETERANS HEALTH ADMINISTRATION · PI WILLIAMS, CHRISTOPHER S. · 2012 to 2024
–
BLRD VA I01 BX001426NIDDK NIH HHS F30 DK120149NIDDK NIH HHS F32 DK108492NIDDK NIH HHS P30 DK058404NIDDK NIH HHS R01 DK099204NIGMS NIH HHS T32 GM007347
6 · The paper itself

Abstract

purpose of reviewMetabolic reprogramming is essential for the rapid proliferation of cancer cells and is thus recognized as a hallmark of cancer. In this review, we will discuss the etiologies and effects of metabolic reprogramming in colorectal cancer. RECENT

findingsChanges in cellular metabolism may precede the acquisition of driver mutations ultimately leading to colonocyte transformation. Oncogenic mutations and loss of tumor suppressor genes further reprogram CRC cells to upregulate glycolysis, glutaminolysis, one-carbon metabolism, and fatty acid synthesis. These metabolic changes are not uniform throughout tumors, as subpopulations of tumor cells may rely on different pathways to adapt to nutrient availability in the local tumor microenvironment. Finally, metabolic cross-communication between stromal cells, immune cells, and the gut microbiota enable CRC growth, invasion, and metastasis. SUMMARY: Altered cellular metabolism occurs in CRC at multiple levels, including in the cells that make up the bulk of CRC tumors, cancer stem cells, the tumor microenvironment, and host-microbiome interactions. This knowledge may inform the development of improved screening and therapeutics for CRC.

Indexed as

Cancer stem cellsColorectal cancerMetabolismMicrobiomeTumor microenvironmentWarburg effect

Identifiers

PMID31406492
PMCPMC6690608
OpenAlexW2901242849

What OpenQuestion holds

Textmetadata
LicenceTDM
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.