Evidence map›Paper›PMID 34047175›Full record

ArticleHaematologica2021

A Pin1/PML/P53 axis activated by retinoic acid in

Rita Hleihel, Hiba El Hajj, Hsin-Chieh Wu, Caroline Berthier, Hong-Hu Zhu, Radwan Massoud, Zaher Chakhachiro, Marwan El Sabban, Hugues De The, Ali Bazarbachi

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Recent advances in AML with mutated NPM1.International journal of hematology · 2024
    Review
  4. Review
  5. Review
  6. Review
  7. The regulatory role of Pin1 in neuronal death.Neural regeneration research · 2023
    Review
  8. Article
  9. Article
  10. A bibliometric analysis of PIN1 and cell death.Frontiers in cell and developmental biology · 2022
    Article
  11. Review
  12. Pulling the Pin on NPMcHaematologica · 2021
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 6 institutions in 4 countries.

Rita HleihelDepartment of Internal Medicine, American University of Beirut, Beirut, Lebanon; Department of Anatomy, Cell Biology and Physiological Sciences, American University of Beirut, Beirut, Lebanon.
Hiba El HajjDepartment of Experimental Pathology, Microbiology and Immunology, Beirut.
Hsin-Chieh WuUniversité de Paris, INSERM UMR 944, CNRS UMR 7212, Equipe labellisée par la Ligue Nationale contre le Cancer, IRSL, Hôpital St. Louis, Paris, College de France, PSL University, CIRB, INSERM UMR 1050, CNRS UMR 7241, Paris.
Caroline BerthierUniversité de Paris, INSERM UMR 944, CNRS UMR 7212, Equipe labellisée par la Ligue Nationale contre le Cancer, IRSL, Hôpital St. Louis, Paris; College de France, PSL University, CIRB, INSERM UMR 1050, CNRS UMR 7241, Paris.
Hong-Hu ZhuDepartment of Hematology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou.
Radwan MassoudDepartment of Internal Medicine, American University of Beirut, Beirut.
Zaher ChakhachiroDepartment of Pathology and Laboratory Medicine, American University of Beirut, Beirut.
Marwan El SabbanDepartment of Anatomy, Cell Biology and Physiological Sciences, American University of Beirut, Beirut.
Hugues De TheUniversité de Paris, INSERM UMR 944, CNRS UMR 7212, Equipe labellisée par la Ligue Nationale contre le Cancer, IRSL, Hôpital St. Louis, Paris; College de France, PSL University, CIRB, INSERM UMR 1050, CNRS UMR 7241, Paris.
Ali BazarbachiDepartment of Internal Medicine, American University of Beirut, Beirut; Department of Anatomy, Cell Biology and Physiological Sciences, American University of Beirut, Beirut. bazarbac@aub.edu.lb.
American University of Beirut · LBCentre National de la Recherche Scientifique · FRCzech Academy of Sciences, Institute of Microbiology · CZInserm · FRLa Ligue Contre le Cancer · FRZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinoic acid (RA) was proposed to increase survival of chemotherapy- treated patients with nucleophosmin-1 (NPM-1c)-mutated acute myeloid leukemia. We reported that, ex vivo, RA triggers NPM-1c degradation, P53 activation and growth arrest. PML organizes domains that control senescence or proteolysis. Here, we demonstrate that PML is required to initiate RA-driven NPM-1c degradation, P53 activation and cell death. Mechanistically, RA enhances PML basal expression through inhibition of activated Pin1, prior to NPM-1c degradation. Such PML induction drives P53 activation, favoring blast response to chemotherapy or arsenic in vivo. This RA/PML/P53 cascade could mechanistically explain RA-facilitated chemotherapy response in patients with NPM-1c mutated acute myeloid leukemia.

Indexed as

Leukemia, Myeloid, AcuteLeukemia, Promyelocytic, AcuteHumansNIMA-Interacting Peptidylprolyl IsomeraseNuclear ProteinsOncogene Proteins, FusionTretinoinTumor Suppressor Protein p53NIMA-Interacting Peptidylprolyl IsomeraseNuclear ProteinsOncogene Proteins, FusionPIN1 protein, humanTretinoinTumor Suppressor Protein p53

Identifiers

PMID34047175
PMCPMC8634200
OpenAlexW3164968883

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.