Evidence map›Paper›PMID 28557977›Full record

ReviewBritish journal of cancer2017

Akt as a target for cancer therapy: more is not always better (lessons from studies in mice).

Qi Wang, Xinyu Chen, Nissim Hay

Open access · hybridAbstract readReview
In one paragraph

Review in British journal of cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

72 citing papers in PubMed, 161 citations in OpenAlex.

  1. Akt isoform specificity drives intrinsic immune regulation during HSV-1 infection.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. AKT kinases as therapeutic targets.Journal of experimental & clinical cancer research : CR · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Strategy toward Kinase-Selective Drug Discovery.Journal of chemical theory and computation · 2023
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. "The emerging role of capivasertib in breast cancer".Breast (Edinburgh, Scotland) · 2022
    Review
  19. Review
  20. NSAIDs and Cancer Resolution: New Paradigms beyond Cyclooxygenase.International journal of molecular sciences · 2022
    Review

12 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

3 authors at 1 institution in 1 country.

Qi WangDepartment of Biochemistry and Molecular Genetics, College of Medicine, University of Illinois at Chicago, Chicago, IL 60607, USA.
Xinyu ChenDepartment of Biochemistry and Molecular Genetics, College of Medicine, University of Illinois at Chicago, Chicago, IL 60607, USA.
Nissim HayDepartment of Biochemistry and Molecular Genetics, College of Medicine, University of Illinois at Chicago, Chicago, IL 60607, USA.
University of Illinois Chicago · US

Funding

PI3K/PTEN/Akt signaling and the genesis of cancerR01CA090764 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Nissim Hay · 2001 to 2026
$9.4M
The Role of Akt in Cell Survival and Cell GrowthR01AG016927 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI HAY, NISSIM · 1998 to 2023
$9.0M
Hexokinase 2 in liver cancerR01CA206167 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI HAY, NISSIM · 2016 to 2020
$2.1M
BLRD VA I01 BX000733NCI NIH HHS R01 CA090764NCI NIH HHS R01 CA206167NIA NIH HHS R01 AG016927
6 · The paper itself

Abstract

The PI3K/Akt signalling pathway is one of the most frequently altered signalling networks in human cancers and has become an attractive target in anticancer therapy. Several drugs targeting this pathway are currently in different phases of clinical trials. However, accumulating reports suggest that adverse effects such as hyperglycaemia and hyperinsulinaemia accompany treatment with pan-PI3K and pan-Akt inhibitors. Thus, understanding the consequences of the systemic deletion or inhibition of Akt activity in vivo is imperative. Three Akt isoforms may individually affect different cancer cells in culture to varying degrees that could suggest specific targeting of different Akt isoforms for different types of cancer. However, the results obtained in cell culture do not address the consequences of Akt isoform inhibition at the organismal level and consequently fail to predict the feasibility of targeting these isoforms for cancer therapy. This review summarises and discusses the consequences of genetic deletions of Akt isoforms in adult mice and their implications for cancer therapy. Whereas combined Akt1 and Akt2 rapidly induced mortality, hepatic Akt inhibition induced liver injury that promotes hepatocellular carcinoma. These findings may explain some of the side effects exerted by pan-PI3K and pan-Akt inhibitors and suggest that close attention must be paid when targeting all Akt isoforms as a therapeutic intervention.

Indexed as

AnimalsCarcinoma, HepatocellularCell ProliferationHumansLiver NeoplasmsMiceMolecular Targeted TherapyPhosphatidylinositol 3-KinasesProtein IsoformsProto-Oncogene Proteins c-aktSignal TransductionAkt1 protein, mouseAkt2 protein, mousePhosphatidylinositol 3-KinasesProtein IsoformsProto-Oncogene Proteins c-akt

Identifiers

PMID28557977
PMCPMC5520506
OpenAlexW2617653110

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.