Evidence map›Paper›PMID 28776567›Full record

ArticleLeukemia2018

Retinoic acid and arsenic trioxide sensitize acute promyelocytic leukemia cells to ER stress.

S Masciarelli, E Capuano, T Ottone, M Divona, S De Panfilis, C Banella, N I Noguera, A Picardi, G Fontemaggi, G Blandino and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
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  4. WTAP and mCellular and molecular life sciences : CMLS · 2024
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  6. Retinoic acid and proteotoxic stress induce AML cell death overcoming stromal cell protection.Journal of experimental & clinical cancer research : CR · 2023
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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

12 authors at 4 institutions in 1 country.

S MasciarelliSection of Histology and Medical Embryology, Department of Anatomical, Histological, Forensic and Orthopedic Sciences, Sapienza University of Rome, Rome, Italy.
E CapuanoSection of Histology and Medical Embryology, Department of Anatomical, Histological, Forensic and Orthopedic Sciences, Sapienza University of Rome, Rome, Italy.
T OttoneDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
M DivonaDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
S De PanfilisCentre for Life Nano Science, Istituto Italiano di Tecnologia, Rome, Italy.
C BanellaLaboratory of Neuro-Oncohematology Unit, Santa Lucia Foundation, Rome, Italy.
N I NogueraDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
A PicardiStem Cell Transplant Unit, Rome Transplant Network, Department of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
G FontemaggiOncogenomic and Epigenetic Unit, Regina Elena National Cancer Institute, Rome, Italy.
G BlandinoOncogenomic and Epigenetic Unit, Regina Elena National Cancer Institute, Rome, Italy.
F Lo-CocoDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
F FaziSection of Histology and Medical Embryology, Department of Anatomical, Histological, Forensic and Orthopedic Sciences, Sapienza University of Rome, Rome, Italy.
University of Rome Tor Vergata · ITSapienza University of Rome · ITFondazione Santa Lucia · ITItalian Institute of Technology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinoic acid (RA) in association with chemotherapy or with arsenic trioxide (ATO) results in high cure rates of acute promyelocytic leukemia (APL). We show that RA-induced differentiation of human leukemic cell lines and primary blasts dramatically increases their sensitivity to endoplasmic reticulum (ER) stress-inducing drugs at doses that are not toxic in the absence of RA. In addition, we demonstrate that the PERK pathway, triggered in response to ER stress, has a major protective role. Moreover, low amounts of pharmacologically induced ER stress are sufficient to strongly increase ATO toxicity. Indeed, in the presence of ER stress, ATO efficiently induced apoptosis in RA-sensitive and RA-resistant APL cell lines, at doses ineffective in the absence of ER stress. Our findings identify the ER stress-related pathways as potential targets in the search for novel therapeutic strategies in AML.

Indexed as

Antineoplastic AgentsApoptosisArsenic TrioxideCell DifferentiationCell LineCell Line, TumorEndoplasmic Reticulum StressHEK293 CellsHumansLeukemia, Promyelocytic, AcuteTretinoinAntineoplastic AgentsArsenic TrioxideTretinoin

Identifiers

PMID28776567
PMCPMC5808088
OpenAlexW2744177318

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.