Evidence map›Paper›PMID 31635329›Full record

ReviewCancers2019

Acute Promyelocytic Leukemia: Update on the Mechanisms of Leukemogenesis, Resistance and on Innovative Treatment Strategies.

N I Noguera, G Catalano, C Banella, M Divona, I Faraoni, T Ottone, W Arcese, M T Voso

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.7field-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.

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

50 citing papers in PubMed, 104 citations in OpenAlex.

  1. Article
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  19. Association betweenThe Journal of international medical research · 2022
    Article
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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

8 authors at 2 institutions in 1 country.

N I NogueraDepartment of Biomedicine and Prevention, Tor Vergata University of Rome, 00133 Rome, Italy. n.noguera@hsantalucia.it.ORCID 0000-0001-7682-862X
G CatalanoDepartment of Biomedicine and Prevention, Tor Vergata University of Rome, 00133 Rome, Italy. gianfranco.catalano@uniroma2.it.
C BanellaDepartment of Biomedicine and Prevention, Tor Vergata University of Rome, 00133 Rome, Italy. cristina.banella@gmail.com.
M DivonaPoliclinico Tor vergata, 00133 Rome, Italy. mariadomenica.divona@ptvonline.it.
I FaraoniDepartment of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy. faraoni@med.uniroma2.it.
T OttoneDepartment of Biomedicine and Prevention, Tor Vergata University of Rome, 00133 Rome, Italy. tiziana.ottone@uniroma2.it.
W ArceseDepartment of Biomedicine and Prevention, Tor Vergata University of Rome, 00133 Rome, Italy. william.arcese@ptvonline.it.
M T VosoDepartment of Biomedicine and Prevention, Tor Vergata University of Rome, 00133 Rome, Italy. Voso@med.uniroma2.it.ORCID 0000-0002-6164-4761
University of Rome Tor Vergata · ITPoliclinico Tor Vergata · IT

Funding

Associazione Italiana per la Ricerca sul Cancro #21267Ministero dell'Istruzione, dell'Università e della Ricerca 2017WXR7ZT
6 · The paper itself

Abstract

This review highlights new findings that have deepened our understanding of the mechanisms of leukemogenesis, therapy and resistance in acute promyelocytic leukemia (APL). Promyelocytic leukemia-retinoic acid receptor α (PML-RARa) sets the cellular landscape of acute promyelocytic leukemia (APL) by repressing the transcription of RARa target genes and disrupting PML-NBs. The RAR receptors control the homeostasis of tissue growth, modeling and regeneration, and PML-NBs are involved in self-renewal of normal and cancer stem cells, DNA damage response, senescence and stress response. The additional somatic mutations in APL mainly involve FLT3, WT1, NRAS, KRAS, ARID1B and ARID1A genes. The treatment outcomes in patients with newly diagnosed APL improved dramatically since the advent of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). ATRA activates the transcription of blocked genes and degrades PML-RARα, while ATO degrades PML-RARa by promoting apoptosis and has a pro-oxidant effect. The resistance to ATRA and ATO may derive from the mutations in the RARa ligand binding domain (LBD) and in the PML-B2 domain of PML-RARa, but such mutations cannot explain the majority of resistances experienced in the clinic, globally accounting for 5-10% of cases. Several studies are ongoing to unravel clonal evolution and resistance, suggesting the therapeutic potential of new retinoid molecules and combinatorial treatments of ATRA or ATO with different drugs acting through alternative mechanisms of action, which may lead to synergistic effects on growth control or the induction of apoptosis in APL cells.

Indexed as

APLascorbateATOATRANGSresistancetherapy

Identifiers

PMID31635329
PMCPMC6826966
OpenAlexW2979672689

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.