Evidence map›Paper›PMID 24344243›Full record

ReviewThe Journal of experimental medicine2013

Synergy against PML-RARa: targeting transcription, proteolysis, differentiation, and self-renewal in acute promyelocytic leukemia.

Guilherme Augusto Dos Santos, Lev Kats, Pier Paolo Pandolfi

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in The Journal of experimental medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05297123 (Treatment of Acute Myeloid Leukemia With Arsenic and All-trans Retinoid Acid), which is not on this map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
6.3field-weighted citation impact, top 3% 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.

NCT05297123 phase1unknown statusnot on this mapstarted 2019, after this paper: background citation

Treatment of Acute Myeloid Leukemia With Arsenic and All-trans Retinoid Acid (ATRA)

TypeinterventionalSponsorFirst Affiliated Hospital Xi'an Jiaotong UniversityRan2019 to 2023Enrolled30ConditionsAcute Myeloid LeukemiaArmsAll-trans retinoic acid, Arsenic Trioxide, Realgar-Indigo naturalis formula
3 · Its place in the literature

Who cites it

81 citing papers in PubMed, 142 citations in OpenAlex.

  1. Article
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  17. Review
  18. Mechanistic update of Trisenox in blood cancer.Current research in pharmacology and drug discovery · 2023
    Review
  19. Review
  20. Article

21 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.

Guilherme Augusto Dos SantosCancer Genetics Program, Beth Israel Deaconess Cancer Center; and 2 Department of Medicine and 3 Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215.
Lev Kats
Pier Paolo Pandolfi
Harvard University · US

Funding

Targeting PML for Leukemia TherapyR01CA142874 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI AVIGAN, DAVID E. · 2010 to 2020
$4.5M
Role of POZ-zinc in hemopoietic malignaciesR01CA102142 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI PANDOLFI, PIER PAOLO · 2004 to 2014
$3.3M
A metabolic role for PML in tumor suppressionR01CA142780 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI PANDOLFI, PIER PAOLO · 2010 to 2014
$1.7M
NCI NIH HHS R01 CA102142NCI NIH HHS R01CA102142NCI NIH HHS R01 CA142780NCI NIH HHS R01CA142780NCI NIH HHS R01 CA142874NCI NIH HHS R01CA142874
6 · The paper itself

Abstract

Acute promyelocytic leukemia (APL) is a hematological malignancy driven by a chimeric oncoprotein containing the C terminus of the retinoic acid receptor-a (RARa) fused to an N-terminal partner, most commonly promyelocytic leukemia protein (PML). Mechanistically, PML-RARa acts as a transcriptional repressor of RARa and non-RARa target genes and antagonizes the formation and function of PML nuclear bodies that regulate numerous signaling pathways. The empirical discoveries that PML-RARa-associated APL is sensitive to both all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO), and the subsequent understanding of the mechanisms of action of these drugs, have led to efforts to understand the contribution of molecular events to APL cell differentiation, leukemia-initiating cell (LIC) clearance, and disease eradication in vitro and in vivo. Critically, the mechanistic insights gleaned from these studies have resulted not only in a better understanding of APL itself, but also carry valuable lessons for other malignancies.

Indexed as

AnimalsArsenicalsArsenic TrioxideCell DifferentiationCell Line, TumorCell Transformation, NeoplasticGene Expression Regulation, LeukemicHumansLeukemia, Promyelocytic, AcuteMiceOncogene Proteins, FusionOxidesRemission InductionSignal TransductionTranscriptional ActivationTretinoinArsenicalsArsenic TrioxideOncogene Proteins, FusionOxidespromyelocytic leukemia-retinoic acid receptor alpha fusion oncoproteinTretinoin

Identifiers

PMID24344243
PMCPMC3865469
OpenAlexW2136199362

What OpenQuestion holds

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Registered trials

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.