Evidence map›Paper›PMID 27919797›Full record

ReviewPharmacology & therapeutics2017

Maximising the potential of AKT inhibitors as anti-cancer treatments.

Jessica S Brown, Udai Banerji

Open access · hybridAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed
11.0field-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

140 citing papers in PubMed, 224 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. AKT and DUBs: a bidirectional relationship.Cellular & molecular biology letters · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. 4(3International journal of molecular sciences · 2025
    Review
  12. Article
  13. Article
  14. Review
  15. Pharmacogenomic andFrontiers in pharmacology · 2025
    Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

80 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

2 authors at 1 institution in 1 country.

Jessica S BrownRoyal Marsden NHS Foundation Trust, London SM2 5PT, UK.
Udai BanerjiRoyal Marsden NHS Foundation Trust, London SM2 5PT, UK; The Institute of Cancer Research, London SM2 5NG, UK. Electronic address: udai.banerji@icr.ac.uk.
Royal Marsden NHS Foundation Trust · GB

Funding

Cancer Research UK 22897
6 · The paper itself

Abstract

PI3K/AKT signalling is commonly disrupted in human cancers, with AKT being a central component of the pathway, influencing multiple processes that are directly involved in tumourigenesis. Targeting AKT is therefore a highly attractive anti-cancer strategy with multiple AKT inhibitors now in various stages of clinical development. In this review, we summarise the role and regulation of AKT signalling in normal cellular physiology. We highlight the mechanisms by which AKT signalling can be hyperactivated in cancers and discuss the past, present and future clinical strategies for AKT inhibition in oncology.

Indexed as

AnimalsAntineoplastic AgentsDrug DesignHumansNeoplasmsPhosphatidylinositol 3-KinaseProtein Kinase InhibitorsProto-Oncogene Proteins c-aktSignal TransductionAntineoplastic AgentsPhosphatidylinositol 3-KinaseProtein Kinase InhibitorsProto-Oncogene Proteins c-aktAKTAKT inhibitorsCancerPI3K/AKT signallingPKB

Identifiers

PMID27919797
PMCPMC6143165
OpenAlexW2557860064

What OpenQuestion holds

Textmetadata
LicenceTDM
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.