Evidence map›Paper›PMID 26233912›Full record

ReviewAdvances in pharmacology (San Diego, Calif.)2015

Role of Retinoic Acid-Metabolizing Cytochrome P450s, CYP26, in Inflammation and Cancer.

Faith Stevison, Jing Jing, Sasmita Tripathy, Nina Isoherranen

Abstract readReview
In one paragraph

Review in Advances in pharmacology (San Diego, Calif.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
9.9field-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

56 citing papers in PubMed, 89 citations in OpenAlex.

  1. Trial
  2. Retinoic acid in health and disease.Signal transduction and targeted therapy · 2026
    Review
  3. Article
  4. Article
  5. Cetyl All-International journal of molecular sciences · 2026
    Article
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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 1 institution in 1 country.

Faith StevisonDepartment of Pharmaceutics, School of Pharmacy, University of Washington, Seattle, Washington, USA.
Jing JingDepartment of Pharmaceutics, School of Pharmacy, University of Washington, Seattle, Washington, USA.
Sasmita TripathyDepartment of Pharmaceutics, School of Pharmacy, University of Washington, Seattle, Washington, USA.
Nina IsoherranenDepartment of Pharmaceutics, School of Pharmacy, University of Washington, Seattle, Washington, USA. Electronic address: ni2@uw.edu.
University of Washington · US

Funding

Mechanisms of Regulation of Retinoic Acid HomeostasisR01GM111772 · NIGMS · UNIVERSITY OF WASHINGTON · PI ISOHERRANEN, NINA · 2014 to 2021
$3.0M
Effects of Xenobiotics on CYP26 Activity and Retinoic Acid HomeostasisR01GM081569 · NIGMS · UNIVERSITY OF WASHINGTON · PI ISOHERRANEN, NINA · 2008 to 2012
$1.7M
NIGMS NIH HHS R01 GM081569NIGMS NIH HHS R01 GM111772
6 · The paper itself

Abstract

Vitamin A (retinol) and its active metabolite, all-trans-retinoic acid (atRA), play critical roles in regulating the differentiation, growth, and migration of immune cells. Similarly, as critical signaling molecules in the regulation of the cell cycle, retinoids are important in cancers. Concentrations of atRA are tightly regulated in tissues, predominantly by the availability of retinol, synthesis of atRA by ALDH1A enzymes and metabolism and clearance of atRA by CYP26 enzymes. The ALDH1A and CYP26 enzymes are expressed in several cell types in the immune system and in cancer cells. In the immune system, the ALDH1A and CYP26 enzymes appear to modulate RA concentrations. Consequently, alterations in the activity of ALDH1A and CYP26 enzymes are expected to change disease outcomes in inflammation. There is increasing evidence from various disease models of intestinal and skin inflammation that treatment with atRA has a positive effect on disease markers. However, whether aberrant atRA concentrations or atRA synthesis and metabolism play a role in inflammatory disease development and progression is not well understood. In cancers, especially in acute promyelocytic leukemia and neuroblastoma, increasing intracellular concentrations of atRA appears to provide clinical benefit. Inhibition of the CYP26 enzymes to increase atRA concentrations and combat therapy resistance has been pursued as a drug target in these cancers. This chapter covers the current knowledge of how atRA and retinol regulate the immune system and inflammation, how retinol and atRA metabolism is altered in inflammation and cancer, and what roles atRA-metabolizing enzymes have in immune responses and cancers.

Indexed as

AnimalsCytochrome P-450 Enzyme SystemHumansImmune SystemInflammationNeoplasmsTretinoinVitamin ACytochrome P-450 Enzyme SystemTretinoinVitamin ACYP26Inflammatory bowel diseaseLeukemiaNeuroblastomaPsoriasisRetinoic acidVitamin A

Identifiers

PMID26233912
PMCPMC4859867
OpenAlexW2419822072

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.