Evidence map›Paper›PMID 24694321›Full record

ReviewExperimental cell research2014

Retinoid receptor signaling and autophagy in acute promyelocytic leukemia.

Nina Orfali, Sharon L McKenna, Mary R Cahill, Lorraine J Gudas, Nigel P Mongan

Abstract readReview
In one paragraph

Review in Experimental cell research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 45 citations in OpenAlex.

  1. Guideline
  2. Guideline
  3. Review
  4. Article
  5. The Question of Survival or Death: What Is the Role of Autophagy in Acute Myeloid Leukemia (AML)?International journal of hematology-oncology and stem cell research · 2022
    Review
  6. Article
  7. Article
  8. All-Frontiers in oncology · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. [Changes in autophagy during maturation and differentiation of Hepa1-6 cells induced by all-trans retinoic acid].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

5 authors at 4 institutions in 3 countries.

Nina OrfaliCork Cancer Research Center, University College Cork, Cork, Ireland; Department of Pharmacology, Weill Cornell Medical College, New York, NY 10065, USA.
Sharon L McKennaCork Cancer Research Center, University College Cork, Cork, Ireland.
Mary R CahillDepartment of Hematology, Cork University Hospital, Cork, Ireland.
Lorraine J GudasDepartment of Pharmacology, Weill Cornell Medical College, New York, NY 10065, USA.. Electronic address: ljgudas@med.cornell.edu.
Nigel P MonganFaculty of Medicine and Health Science, School of Veterinary Medicine and Science, University of Nottingham, LE12 5RD, United Kingdom; Department of Pharmacology, Weill Cornell Medical College, New York, NY 10065, USA.. Electronic address: nigel.mongan@nottingham.ac.uk.
Cornell University · USCork University Hospital · IEUniversity College Cork · IEUniversity of Nottingham · GB

Funding

Retinoic Acid Binding Proteins: Functional StudiesR01CA043796 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI GUDAS, LORRAINE J · 1987 to 2013
$5.0M
NCI NIH HHS R01 CA043796NCI NIH HHS R01CA43796
6 · The paper itself

Abstract

Retinoids are a family of signaling molecules derived from vitamin A with well established roles in cellular differentiation. Physiologically active retinoids mediate transcriptional effects on cells through interactions with retinoic acid (RARs) and retinoid-X (RXR) receptors. Chromosomal translocations involving the RARα gene, which lead to impaired retinoid signaling, are implicated in acute promyelocytic leukemia (APL). All-trans-retinoic acid (ATRA), alone and in combination with arsenic trioxide (ATO), restores differentiation in APL cells and promotes degradation of the abnormal oncogenic fusion protein through several proteolytic mechanisms. RARα fusion-protein elimination is emerging as critical to obtaining sustained remission and long-term cure in APL. Autophagy is a degradative cellular pathway involved in protein turnover. Both ATRA and ATO also induce autophagy in APL cells. Enhancing autophagy may therefore be of therapeutic benefit in resistant APL and could broaden the application of differentiation therapy to other cancers. Here we discuss retinoid signaling in hematopoiesis, leukemogenesis, and APL treatment. We highlight autophagy as a potential important regulator in anti-leukemic strategies.

Indexed as

Leukemia, Promyelocytic, AcuteAnimalsAutophagyCell DifferentiationHematopoiesisHumansReceptors, Retinoic AcidRetinoidsSignal TransductionReceptors, Retinoic AcidRetinoidsAMLAPLArsenic trioxideATRAAutophagyDifferentiationHematopoiesisPML–RARαRetinoid

Identifiers

PMID24694321
PMCPMC4047711
OpenAlexW1970521215

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.