Evidence map›Paper›PMID 14576840›Full record

ReviewOncogene2003

Retinoids in cancer therapy and chemoprevention: promise meets resistance.

Sarah J Freemantle, Michael J Spinella, Ethan Dmitrovsky

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed, 2 pooled it
6.7field-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

118 citing papers in PubMed, 2 syntheses or guidelines pooled it, 314 citations in OpenAlex.

  1. Pooled it
  2. Treatment for Barrett's oesophagus.The Cochrane database of systematic reviews · 2010
    Pooled it
  3. Trial
  4. Retinoic acid-loaded nanoparticles enhance macrophage-mediated control ofTurkish journal of biology = Turk biyoloji dergisi · 2026
    Article
  5. Review
  6. Evolutionary conservation and cancer implications of the WNT signaling pathway.Medical oncology (Northwood, London, England) · 2025
    Review
  7. Review
  8. Review
  9. Article
  10. All-Trans Retinoic Acid Effect onJournal of fungi (Basel, Switzerland) · 2022
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Retinoids as Chemo-Preventive and Molecular-Targeted Anti-Cancer Therapies.International journal of molecular sciences · 2021
    Review
  18. Review
  19. Review
  20. Review

58 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.

Sarah J FreemantleDepartment of Pharmacology and Toxicology, Dartmouth Medical School, Hanover, NH 03755, USA. sarah.freemantle@dartmouth.edu
Michael J Spinella
Ethan Dmitrovsky
Dartmouth College · US

Funding

RETINOID CANCER PREVENTION MECHANISMSR01CA087546 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DMITROVSKY, ETHAN · 2000 to 2015
$4.1M
RETINOIC ACID PARADOX AND PROMYELOCYTIC LEUKEMIAR01CA062275 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI DMITROVSKY, ETHAN · 1994 to 2013
$2.9M
RETINOID INDUCED TUMOR DIFFERENTIATION AND THE CELL CYCLK01CA075154 · NCI · DARTMOUTH COLLEGE · PI SPINELLA, MICHAEL J · 1998 to 2002
$408k
NCI NIH HHS K01 CA 75154-01NCI NIH HHS R01 CA062275NCI NIH HHS R01 CA 62275NCI NIH HHS R01 CA 87546
6 · The paper itself

Abstract

Retinoids (natural and synthetic derivatives of vitamin A) signal potent differentiation and growth-suppressive effects in diverse normal, premalignant, and malignant cells. A strong rationale exists for the use of retinoids in cancer treatment and chemoprevention based on preclinical, epidemiological, and early clinical findings. Despite the success of all-trans-retinoic acid (RA)-based differentiation therapy in acute promyelocytic leukemia (APL), the broad promise of retinoids in the clinic has not yet been realized. In addition to the expected limited activity of any single therapeutic agent, translation of retinoid activities from the laboratory to the clinic has met with intrinsic or acquired retinoid resistance. Evidence suggests that solid tumors develop intrinsic resistance to retinoids during carcinogenesis. In contrast, relapse of APL is often associated with acquired resistance to retinoid maturation induction. This review discusses what is known about retinoid resistance mechanisms in cancer therapy and chemoprevention. Strategies to overcome this resistance will be discussed, including combination therapy with other differentiation-inducing, cytotoxic or chromatin-remodeling agents, as well as the use of receptor-selective and nonclassical retinoids. Opportunities exist in the post-genomic era to bypass resistance to classical retinoids by identifying target genes and associated pathways that directly mediate the antineoplastic effects of retinoids. In this regard, the retinoids are useful pharmacological tools to reveal important pathways targeted in cancer therapy and chemoprevention.

Indexed as

Drug Resistance, NeoplasmHumansLeukemia, Promyelocytic, AcuteNeoplasmsReceptors, Retinoic AcidRetinoidsTumor Suppressor ProteinsReceptors, Retinoic AcidRetinoidsTumor Suppressor Proteins

Identifiers

PMID14576840
OpenAlexW2040347441

What OpenQuestion 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 OpenQuestion graph.