Evidence map›Paper›PMID 29880805›Full record

ArticleCell death & disease2018

Pharmacological inactivation of the PI3K p110δ prevents breast tumour progression by targeting cancer cells and macrophages.

Evangelia Goulielmaki, Miriam Bermudez-Brito, Margarita Andreou, Niki Tzenaki, Maria Tzardi, Eelco de Bree, Eleftheria Tsentelierou, Antonis Makrigiannakis, Evangelia A Papakonstanti

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. 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
1.6field-weighted citation impact, top 13% 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, 52 citations in OpenAlex.

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  11. The Importance of Phosphoinositide 3-Kinase in Neuroinflammation.International journal of molecular sciences · 2024
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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 2 institutions in 1 country.

Evangelia GoulielmakiDepartment of Biochemistry, School of Medicine, University of Crete, Heraklion, Greece.
Miriam Bermudez-BritoDepartment of Biochemistry, School of Medicine, University of Crete, Heraklion, Greece.
Margarita AndreouDepartment of Biochemistry, School of Medicine, University of Crete, Heraklion, Greece.
Niki TzenakiDepartment of Biochemistry, School of Medicine, University of Crete, Heraklion, Greece.
Maria TzardiDepartment of Pathology, University Hospital, School of Medicine, University of Crete, Heraklion, Greece.
Eelco de BreeDepartment of Surgical Oncology, University Hospital, School of Medicine, University of Crete, Heraklion, Greece.
Eleftheria TsentelierouDepartment of Obstetrics and Gynaecology, University Hospital, School of Medicine, University of Crete, Heraklion, Greece.
Antonis MakrigiannakisDepartment of Obstetrics and Gynaecology, University Hospital, School of Medicine, University of Crete, Heraklion, Greece.
Evangelia A PapakonstantiDepartment of Biochemistry, School of Medicine, University of Crete, Heraklion, Greece. epapak@uoc.gr.
University of Crete · GRUniversity Hospital of Heraklion · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patient selection for PI3K-targeted solid cancer treatment was based on the PIK3CA/PTEN mutational status. However, it is increasingly clear that this is not a good predictor of the response of breast cancer cells to the anti-proliferative effect of PI3K inhibitors, indicating that isoform(s) other than p110α may modulate cancer cells sensitivity to PI3K inhibition. Surprisingly, we found that although no mutations in the p110δ subunit have been detected thus far in breast cancer, the expression of p110δ becomes gradually elevated during human breast cancer progression from grade I to grade III. Moreover, pharmacological inactivation of p110δ in mice abrogated the formation of tumours and the recruitment of macrophages to tumour sites and strongly affected the survival, proliferation and apoptosis of grafted tumour cells. Pharmacological inactivation of p110δ in mice with defective macrophages or in mice with normal macrophages but grafted with p110δ-lacking tumours suppressed only partly tumour growth, indicating a requisite role of p110δ in both macrophages and cancer cells in tumour progression. Adoptive transfer of δ

Indexed as

Disease ProgressionAdenineAnimalsApoptosisBreast NeoplasmsCell Line, TumorCell ProliferationCell SurvivalClass Ia Phosphatidylinositol 3-KinaseEnzyme ActivationFemaleHumansMacrophagesMice, Inbred BALB CNeoplasm MetastasisNeoplasm StagingAdenineClass Ia Phosphatidylinositol 3-KinaseIC 87114PTEN PhosphohydrolasePTEN protein, humanQuinazolines

Identifiers

PMID29880805
PMCPMC5992183
OpenAlexW2806253608

What OpenQuestion holds

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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.