Evidence map›Paper›PMID 34033220›Full record

ArticleEMBO molecular medicine2021

Pancreatic cancer intrinsic PI3Kα activity accelerates metastasis and rewires macrophage component.

Benoit Thibault, Fernanda Ramos-Delgado, Elvire Pons-Tostivint, Nicole Therville, Celia Cintas, Silvia Arcucci, Stephanie Cassant-Sourdy, Gabriela Reyes-Castellanos, Marie Tosolini, Amelie V Villard and 16 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2021. 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
2.4field-weighted citation impact, top 8% 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, 42 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

26 authors at 4 institutions in 3 countries.

Benoit ThibaultCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.ORCID 0000-0003-3250-1988
Fernanda Ramos-DelgadoCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.
Elvire Pons-TostivintCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.
Nicole ThervilleCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.
Celia CintasCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.
Silvia ArcucciCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.
Stephanie Cassant-SourdyCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.
Gabriela Reyes-CastellanosAix Marseille Univ, CNRS, INSERM, Institut Paoli-Calmettes, CRCM, Marseille, France.
Marie TosoliniCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.ORCID 0000-0001-5278-5952
Amelie V VillardCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.
Coralie CayronCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.
Romain BaerCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.
Justine Bertrand-MichelLipidomics, I2MC, Inserm, Toulouse, France.
Delphine PaganCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.
Dina Ferreira Da MotaCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.
Hongkai YanDivision of Translational Cancer Research, German Cancer Research Center (DKFZ) and German Cancer Consortium (DKTK), Heidelberg, Germany.
Chiara FalcomatàDivision of Translational Cancer Research, German Cancer Research Center (DKFZ) and German Cancer Consortium (DKTK), Heidelberg, Germany.
Fabrice MuscariCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.
Barbara BournetCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.
Jean-Pierre DelordCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.
Ezra AksoyCentre for Biochemical Pharmacology, William Harvey Research Institute, Queen Mary University of London, London, UK.
Alice CarrierAix Marseille Univ, CNRS, INSERM, Institut Paoli-Calmettes, CRCM, Marseille, France.ORCID 0000-0001-6599-9642
Pierre CordelierCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.
Dieter SaurDivision of Translational Cancer Research, German Cancer Research Center (DKFZ) and German Cancer Consortium (DKTK), Heidelberg, Germany.ORCID 0000-0001-5874-0210
Celine BassetCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.
Julie Guillermet-GuibertCentre de Recherches en Cancérologie de Toulouse, Inserm, CNRS, Université de Toulouse, Toulouse, France.ORCID 0000-0003-3173-4907
Centre National de la Recherche Scientifique · FRGerman Cancer Research Center · DEInserm · FRQueen Mary University of London · GB

Funding

European Research Council 648521
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) patients frequently suffer from undetected micro-metastatic disease. This clinical situation would greatly benefit from additional investigation. Therefore, we set out to identify key signalling events that drive metastatic evolution from the pancreas. We searched for a gene signature that discriminate localised PDAC from confirmed metastatic PDAC and devised a preclinical protocol using circulating cell-free DNA (cfDNA) as an early biomarker of micro-metastatic disease to validate the identification of key signalling events. An unbiased approach identified, amongst actionable markers of disease progression, the PI3K pathway and a distinctive PI3Kα activation signature as predictive of PDAC aggressiveness and prognosis. Pharmacological or tumour-restricted genetic PI3Kα-selective inhibition prevented macro-metastatic evolution by hindering tumoural cell migratory behaviour independently of genetic alterations. We found that PI3Kα inhibition altered the quantity and the species composition of the produced lipid second messenger PIP

Indexed as

AdenocarcinomaCarcinoma, Pancreatic DuctalPancreatic NeoplasmsHumansMacrophagesPhosphatidylinositol 3-KinasesPhosphatidylinositol 3-Kinasespancreatic cancerphosphoinositidePI3K isoformstargeted therapytumour-stroma dialog

Identifiers

PMID34033220
PMCPMC8261517
OpenAlexW3164044183

What OpenQuestion holds

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LicenceCC BY
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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.