Evidence map›Paper›PMID 26338968›Full record

ArticleOncotarget2015

Targeting autophagy enhances the anti-tumoral action of crizotinib in ALK-positive anaplastic large cell lymphoma.

Géraldine Mitou, Julie Frentzel, Aurore Desquesnes, Sophie Le Gonidec, Talal AlSaati, Isabelle Beau, Laurence Lamant, Fabienne Meggetto, Estelle Espinos, Patrice Codogno and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 49 citations in OpenAlex.

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  15. Regulation of Beclin 1-Mediated Autophagy by Oncogenic Tyrosine Kinases.International journal of molecular sciences · 2020
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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.

Géraldine MitouInserm, UMR1037 CRCT, F-31000 Toulouse, France.
Julie FrentzelInserm, UMR1037 CRCT, F-31000 Toulouse, France.
Aurore DesquesnesPhenotyping Service, INSERM-US006 ANEXPLO/CREFRE, Toulouse, France.
Sophie Le GonidecPhenotyping Service, INSERM-US006 ANEXPLO/CREFRE, Toulouse, France.
Talal AlSaatiINSERM/UPS - US006/CREFRE, Service d'Histopathologie, CHU Purpan, Toulouse, France.
Isabelle BeauINSERM UMRS 1185, Faculté de Médecine Paris Sud, Le Kremlin-Bicêtre, France.
Laurence LamantInserm, UMR1037 CRCT, F-31000 Toulouse, France.
Fabienne MeggettoInserm, UMR1037 CRCT, F-31000 Toulouse, France.
Estelle EspinosInserm, UMR1037 CRCT, F-31000 Toulouse, France.
Patrice CodognoInstitut Necker Enfants-Malades, INSERM U1151-CNRS UMR 8253, Paris, France.
Pierre BroussetInserm, UMR1037 CRCT, F-31000 Toulouse, France.
Sylvie GiuriatoInserm, UMR1037 CRCT, F-31000 Toulouse, France.
Inserm · FRCentre National de la Recherche Scientifique · FRUniversité Toulouse III - Paul Sabatier · FRCentre de Recherche en Cancérologie de Toulouse · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anaplastic Lymphoma Kinase-positive Anaplastic Large Cell Lymphomas (ALK+ ALCL) occur predominantly in children and young adults. Their treatment, based on aggressive chemotherapy, is not optimal since ALCL patients can still expect a 30% 2-year relapse rate. Tumor relapses are very aggressive and their underlying mechanisms are unknown. Crizotinib is the most advanced ALK tyrosine kinase inhibitor and is already used in clinics to treat ALK-associated cancers. However, crizotinib escape mechanisms have emerged, thus preventing its use in frontline ALCL therapy. The process of autophagy has been proposed as the next target for elimination of the resistance to tyrosine kinase inhibitors. In this study, we investigated whether autophagy is activated in ALCL cells submitted to ALK inactivation (using crizotinib or ALK-targeting siRNA). Classical autophagy read-outs such as autophagosome visualization/quantification by electron microscopy and LC3-B marker turn-over assays were used to demonstrate autophagy induction and flux activation upon ALK inactivation. This was demonstrated to have a cytoprotective role on cell viability and clonogenic assays following combined ALK and autophagy inhibition. Altogether, our results suggest that co-treatment with crizotinib and chloroquine (two drugs already used in clinics) could be beneficial for ALK-positive ALCL patients.

Indexed as

Anaplastic Lymphoma KinaseAnimalsAntineoplastic Combined Chemotherapy ProtocolsAutophagyCell Line, TumorCell SurvivalChloroquineCrizotinibDose-Response Relationship, DrugDrug SynergismFemaleHumansLymphoma, Large-Cell, AnaplasticMice, Inbred NODMice, SCIDMicrotubule-Associated ProteinsALK protein, humanAlk protein, mouseAnaplastic Lymphoma KinaseChloroquineCrizotinibMAP1LC3B protein, humanMicrotubule-Associated ProteinsProtein Kinase InhibitorsPyrazolesPyridinesReceptor Protein-Tyrosine Kinasesanaplastic large cell lymphomaautophagycrizotinibcytoprotectionNPM-ALK

Identifiers

PMID26338968
PMCPMC4745787
OpenAlexW2147057532

What OpenQuestion 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 OpenQuestion graph.