Evidence map›Paper›PMID 27604463›Full record

ArticleJournal of translational medicine2016

Repositioning of bromocriptine for treatment of acute myeloid leukemia.

María Carmen Lara-Castillo, Josep Maria Cornet-Masana, Amaia Etxabe, Antònia Banús-Mulet, Miguel Ángel Torrente, Meritxell Nomdedeu, Marina Díaz-Beyá, Jordi Esteve, Ruth M Risueño

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

María Carmen Lara-CastilloCentre Esther Koplowitz, Josep Carreras Leukaemia Research Institute, Campus Clínic-University of Barcelona, Rosselló 149-153, 08036, Barcelona, Spain.
Josep Maria Cornet-MasanaCentre Esther Koplowitz, Josep Carreras Leukaemia Research Institute, Campus Clínic-University of Barcelona, Rosselló 149-153, 08036, Barcelona, Spain.
Amaia EtxabeCentre Esther Koplowitz, Josep Carreras Leukaemia Research Institute, Campus Clínic-University of Barcelona, Rosselló 149-153, 08036, Barcelona, Spain.
Antònia Banús-MuletCentre Esther Koplowitz, Josep Carreras Leukaemia Research Institute, Campus Clínic-University of Barcelona, Rosselló 149-153, 08036, Barcelona, Spain.
Miguel Ángel TorrenteCentre Esther Koplowitz, Josep Carreras Leukaemia Research Institute, Campus Clínic-University of Barcelona, Rosselló 149-153, 08036, Barcelona, Spain.
Meritxell NomdedeuCentre Esther Koplowitz, Josep Carreras Leukaemia Research Institute, Campus Clínic-University of Barcelona, Rosselló 149-153, 08036, Barcelona, Spain.
Marina Díaz-BeyáCentre Esther Koplowitz, Josep Carreras Leukaemia Research Institute, Campus Clínic-University of Barcelona, Rosselló 149-153, 08036, Barcelona, Spain.
Jordi EsteveCentre Esther Koplowitz, Josep Carreras Leukaemia Research Institute, Campus Clínic-University of Barcelona, Rosselló 149-153, 08036, Barcelona, Spain.
Ruth M RisueñoCentre Esther Koplowitz, Josep Carreras Leukaemia Research Institute, Campus Clínic-University of Barcelona, Rosselló 149-153, 08036, Barcelona, Spain. risueno@carrerasresearch.org.ORCID 0000-0003-4048-9536
Josep Carreras Leukaemia Research Institute · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTreatment for acute myeloid leukemia (AML) has not significantly changed in the last decades and new therapeutic approaches are needed to achieve prolonged survival rates. Leukemia stem cells (LSC) are responsible for the initiation and maintenance of AML due to their stem-cell properties. Differentiation therapies aim to abrogate the self-renewal capacity and diminish blast lifespan.

methodsAn in silico screening was designed to search for FDA-approved small molecules that potentially induce differentiation of AML cells. Bromocriptine was identified and validated in an in vitro screening. Bromocriptine is an approved drug originally indicated for Parkinson's disease, acromegaly, hyperprolactinemia and galactorrhoea, and recently repositioned for diabetes mellitus.

resultsTreatment with bromocriptine reduced cell viability of AML cells by activation of the apoptosis program and induction of myeloid differentiation. Moreover, the LSC-enriched primitive AML cell fraction was more sensitive to the presence of bromocriptine. In fact, bromocriptine decreased the clonogenic capacity of AML cells. Interestingly, a negligible effect is observed in healthy blood cells and hematopoietic stem/progenitor cells.

conclusionsOur results support the use of bromocriptine as an anti-AML drug in a repositioning setting and the further clinical validation of this preclinical study.

Indexed as

Drug RepositioningAdultBromocriptineCD11b AntigenCell Line, TumorCell SurvivalFemaleHumansLeukemia, Myeloid, AcuteMaleMiddle AgedYoung AdultBromocriptineCD11b AntigenAMLBromocriptineDrug repositioningLeukemia stem cellsNew drug

Identifiers

PMID27604463
PMCPMC5015257
OpenAlexW2516496914

What OpenQuestion holds

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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.