Evidence map›Paper›PMID 26970124›Full record

ReviewSeminars in oncology2016

Retinoids and rexinoids in cancer prevention: from laboratory to clinic.

Iván P Uray, Ethan Dmitrovsky, Powel H Brown

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
7.2field-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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Triorganotin compounds as emerging nuclear retinoid X receptor ligands and their implications in cancer.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. IRX4204 Induces Senescence and Cell Death in HER2-positive Breast Cancer and Synergizes with Anti-HER2 Therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  19. Review
  20. Review

15 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 1 institution in 1 country.

Iván P UrayDepartment of Clinical Cancer Prevention, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA. Electronic address: ivanpeteruray@gmail.com.
Ethan DmitrovskyDepartment of Clinical Cancer Prevention, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Powel H BrownDepartment of Clinical Cancer Prevention, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
RETINOID CANCER PREVENTION MECHANISMSR01CA087546 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DMITROVSKY, ETHAN · 2000 to 2015
$4.1M
PREVENTION OF BREAST CANCER USING SELECTIVE RETINOIDSR01CA078480 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BROWN, POWEL H · 1999 to 2008
$3.1M
RETINOIC ACID PARADOX AND PROMYELOCYTIC LEUKEMIAR01CA062275 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI DMITROVSKY, ETHAN · 1994 to 2013
$2.9M
Cyclin D as a Retinoid Molecular TargetR01CA111422 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DMITROVSKY, ETHAN · 2005 to 2014
$2.7M
Targeting Anaphase Catastrophe to Combat Lung CancerR01CA190722 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KURIE, JONATHAN M · 2015 to 2019
$1.8M
Targeting the lipid synthesis enzyme, DGAT1, for breast cancer preventionR03CA180550 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI URAY, IVAN PETER · 2013 to 2014
$158k
NCI NIH HHS P30 CA016672NCI NIH HHS P30CA16672NCI NIH HHS R01 CA062275NCI NIH HHS R01-CA062275NCI NIH HHS R01 CA078480NCI NIH HHS R01 CA087546NCI NIH HHS R01-CA087546NCI NIH HHS R01 CA111422NCI NIH HHS R01 CA190722NCI NIH HHS R01-CA190722NCI NIH HHS R03 CA180550NCI NIH HHS R03CA180550PHS HHS R01-078480
6 · The paper itself

Abstract

Early in the age of modern medicine the consequences of vitamin A deficiency drew attention to the fundamental link between retinoid-dependent homeostatic regulation and malignant hyperproliferative diseases. The term "retinoid" includes a handful of endogenous and a large group of synthetic derivatives of vitamin A. These multifunctional lipid-soluble compounds directly regulate target genes of specific biological functions and critical signaling pathways to orchestrate complex functions from vision to development, metabolism, and inflammation. Many of the retinoid activities on the cellular level have been well characterized and translated to the regulation of processes like differentiation and cell death, which play critical roles in the outcome of malignant transformation of tissues. In fact, retinoid-based differentiation therapy of acute promyelocytic leukemia was one of the first successful examples of molecularly targeted treatment strategies. The selectivity, high receptor binding affinity and the ability of retinoids to directly modulate gene expression programs present a distinct pharmacological opportunity for cancer treatment and prevention. However, to fully exploit their potential, the adverse effects of retinoids must be averted. In this review we provide an overview of the biology of retinoid (activated by nuclear retinoic acid receptors [RARs]) and rexinoid (engaged by nuclear retinoid X receptors [RXRs]) action concluded from a long line of preclinical studies, in relation to normal and transformed states of cells. We will also discuss the past and current uses of retinoids in the treatment of malignancies, the potential of rexinoids in the cancer prevention setting, both as single agents and in combinations.

Indexed as

Signal TransductionAnimalsAnticarcinogenic AgentsChemopreventionHumansNeoplasmsNervous System DiseasesPulmonary Disease, Chronic ObstructiveReceptors, Retinoic AcidRetinoidsRetinoid X ReceptorsSkin DiseasesAnticarcinogenic AgentsReceptors, Retinoic AcidRetinoidsRetinoid X ReceptorsCancer preventionCombinationMedical useRetinoidRexinoid

Identifiers

PMID26970124
PMCPMC4789177
OpenAlexW2182224080

What OpenQuestion holds

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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.