Evidence map›Paper›PMID 27374081›Full record

ArticleOncotarget2016

Targeting mTOR pathway inhibits tumor growth in different molecular subtypes of triple-negative breast cancers.

Rana Hatem, Rania El Botty, Sophie Chateau-Joubert, Jean-Luc Servely, Dalila Labiod, Ludmilla de Plater, Franck Assayag, Florence Coussy, Céline Callens, Sophie Vacher and 5 more

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Review
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  7. Targeting the mTOR Pathway for the Prevention of ER-Negative Breast Cancer.Cancer prevention research (Philadelphia, Pa.) · 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

15 authors.

Rana HatemGenetics Department, Institut Curie, PSL Research University, Paris, France.
Rania El BottyTranslational Research Department, Institut Curie, PSL Research University, Paris, France.
Sophie Chateau-JoubertBioPôle Alfort, National Veterinary School of Alfort, Maisons Alfort, France.
Jean-Luc ServelyBioPôle Alfort, National Veterinary School of Alfort, Maisons Alfort, France.
Dalila LabiodTranslational Research Department, Institut Curie, PSL Research University, Paris, France.
Ludmilla de PlaterTranslational Research Department, Institut Curie, PSL Research University, Paris, France.
Franck AssayagTranslational Research Department, Institut Curie, PSL Research University, Paris, France.
Florence CoussyGenetics Department, Institut Curie, PSL Research University, Paris, France.
Céline CallensGenetics Department, Institut Curie, PSL Research University, Paris, France.
Sophie VacherGenetics Department, Institut Curie, PSL Research University, Paris, France.
Fabien ReyalTranslational Research Department, Institut Curie, PSL Research University, Paris, France.
Sabina CosulichAstraZeneca R&D Cambr idge, CRUK Cambridge Institute, Cambridge, UK.
Véronique DiérasMedical Oncology Department, Institut Curie, PSL Research University, Paris, France.
Ivan BiècheGenetics Department, Institut Curie, PSL Research University, Paris, France.
Elisabetta MarangoniTranslational Research Department, Institut Curie, PSL Research University, Paris, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple-negative breast cancers (TNBC) are characterized by frequent alterations in the PI3K/AKT/mTOR signaling pathway. In this study, we analyzed PI3K pathway activation in 67 patient-derived xenografts (PDX) of breast cancer and investigated the anti-tumor activity of the mTOR inhibitor everolimus in 15 TNBC PDX with different expression and mutational status of PI3K pathway markers. Expression of the tumor suppressors PTEN and INPP4B was lost in 55% and 76% of TNBC PDX, respectively, while mutations in PIK3CA and AKT1 genes were rare. In 7 PDX treatment with everolimus resulted in a tumor growth inhibition higher than 50%, while 8 models were classified as low responder or resistant. Basal-like, LAR (Luminal AR), mesenchymal and HER2-enriched tumors were present in both responder and resistant groups, suggesting that tumor response to everolimus is not restricted to a specific TNBC subtype. Analysis of treated tumors showed a correlation between tumor response and post-treatment phosphorylation of AKT, increased in responder PDX, while PI3K pathway markers at baseline were not sufficient to predict everolimus response. In conclusion, targeting mTOR decreased tumor growth in 7 out of 15 TNBC PDX tested. Response to everolimus occurred in different TNBC subtypes and was associated with post-treatment increase of P-AKT.

Indexed as

AnimalsCell Growth ProcessesCell Line, TumorDisease Models, AnimalEverolimusFemaleHumansMiceMice, NudeMolecular Targeted TherapySignal TransductionTOR Serine-Threonine KinasesTriple Negative Breast NeoplasmsXenograft Model Antitumor AssaysEverolimusMTOR protein, humanTOR Serine-Threonine KinasesmTORPDXPI3K pathwayTNBC

Identifiers

PMID27374081
PMCPMC5217012

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Registered trials

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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.