Evidence map›Paper›PMID 32630372›Full record

ReviewInternational journal of molecular sciences2020

The PI3K-AKT-mTOR Pathway and Prostate Cancer: At the Crossroads of AR, MAPK, and WNT Signaling.

Boris Y Shorning, Manisha S Dass, Matthew J Smalley, Helen B Pearson

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 365 papers.

0numbers the graph read from it
0cells of the map it votes in
365citing papers in PubMed
26.3field-weighted citation impact, top 1% 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

365 citing papers in PubMed, 587 citations in OpenAlex.

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  18. Network Pharmacology and Molecular Docking ofInternational journal of molecular sciences · 2026
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305 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Boris Y ShorningThe European Cancer Stem Cell Research Institute, Cardiff University, Hadyn Ellis Building, Maindy Road, Cardiff CF24 4HQ, Wales, UK.
Manisha S DassThe European Cancer Stem Cell Research Institute, Cardiff University, Hadyn Ellis Building, Maindy Road, Cardiff CF24 4HQ, Wales, UK.
Matthew J SmalleyThe European Cancer Stem Cell Research Institute, Cardiff University, Hadyn Ellis Building, Maindy Road, Cardiff CF24 4HQ, Wales, UK.ORCID 0000-0001-9540-1146
Helen B PearsonThe European Cancer Stem Cell Research Institute, Cardiff University, Hadyn Ellis Building, Maindy Road, Cardiff CF24 4HQ, Wales, UK.
Cardiff University · GB

Funding

Cancer Research UK 27894Cancer Research UK A27894
6 · The paper itself

Abstract

Oncogenic activation of the phosphatidylinositol-3-kinase (PI3K), protein kinase B (PKB/AKT), and mammalian target of rapamycin (mTOR) pathway is a frequent event in prostate cancer that facilitates tumor formation, disease progression and therapeutic resistance. Recent discoveries indicate that the complex crosstalk between the PI3K-AKT-mTOR pathway and multiple interacting cell signaling cascades can further promote prostate cancer progression and influence the sensitivity of prostate cancer cells to PI3K-AKT-mTOR-targeted therapies being explored in the clinic, as well as standard treatment approaches such as androgen-deprivation therapy (ADT). However, the full extent of the PI3K-AKT-mTOR signaling network during prostate tumorigenesis, invasive progression and disease recurrence remains to be determined. In this review, we outline the emerging diversity of the genetic alterations that lead to activated PI3K-AKT-mTOR signaling in prostate cancer, and discuss new mechanistic insights into the interplay between the PI3K-AKT-mTOR pathway and several key interacting oncogenic signaling cascades that can cooperate to facilitate prostate cancer growth and drug-resistance, specifically the androgen receptor (AR), mitogen-activated protein kinase (MAPK), and WNT signaling cascades. Ultimately, deepening our understanding of the broader PI3K-AKT-mTOR signaling network is crucial to aid patient stratification for PI3K-AKT-mTOR pathway-directed therapies, and to discover new therapeutic approaches for prostate cancer that improve patient outcome.

Indexed as

Androgen AntagonistsCell Line, TumorCell ProliferationHumansMaleMitogen-Activated Protein KinasesNeoplasm Recurrence, LocalOncogenesPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProstatic NeoplasmsProto-Oncogene Proteins c-aktReceptors, AndrogenTOR Serine-Threonine KinasesWnt Signaling PathwayAndrogen AntagonistsAR protein, humanMitogen-Activated Protein KinasesMTOR protein, humanPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktReceptors, AndrogenTOR Serine-Threonine KinasesAKTARcastration-resistant prostate cancer (CRPC)MAPKmTORPI3Kprostate cancertherapeutic resistanceWNT

Identifiers

PMID32630372
PMCPMC7350257
OpenAlexW3037348089

What Socratic 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 Socratic graph.