Evidence map›Paper›PMID 21772331›Full record

ReviewBritish journal of cancer2011

Oncogenic AKTivation of translation as a therapeutic target.

A C Hsieh, M L Truitt, D Ruggero

Open access · hybridAbstract readReview
In one paragraph

Review in British journal of cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

44 citing papers in PubMed, 78 citations in OpenAlex.

  1. Trial
  2. Downregulation of AKT-mediated p27IBRO neuroscience reports · 2025
    Article
  3. Article
  4. Review
  5. Purinergic P2X7R as a potential target for pancreatic cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Revealing nascent proteomics in signaling pathways and cell differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
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 2 institutions in 1 country.

A C HsiehDepartment of Urology, School of Medicine, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, Helen Diller Family Cancer Research Building, Room 386, 1450 3rd Street, San Francisco, CA 94158-3110, USA.
M L Truitt
D Ruggero
University of California, San Francisco · USUCSF Helen Diller Family Comprehensive Cancer Center · US

Funding

The role of deregulated protein synthesis control in Myc-induced tumorigenesisR01CA140456 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUGGERO, DAVIDE · 2009 to 2019
$3.3M
Role of rRNA Modifications in Dyskeratosis Congenita and Translation ControlR01HL085572 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUGGERO, DAVIDE · 2006 to 2009
$1.8M
NCI NIH HHS R01 CA140456NHLBI NIH HHS R01 HL085572
6 · The paper itself

Abstract

The AKT signalling pathway is a major regulator of protein synthesis that impinges on multiple cellular processes frequently altered in cancer, such as proliferation, cell growth, survival, and angiogenesis. AKT controls protein synthesis by regulating the multistep process of mRNA translation at every stage from ribosome biogenesis to translation initiation and elongation. Recent studies have highlighted the ability of oncogenic AKT to drive cellular transformation by altering gene expression at the translational level. Oncogenic AKT signalling leads to both global changes in protein synthesis as well as specific changes in the translation of select mRNAs. New and developing technologies are significantly advancing our ability to identify and functionally group these translationally controlled mRNAs into gene networks based on their modes of regulation. How oncogenic AKT activates ribosome biogenesis, translation initiation, and translational elongation to regulate these translational networks is an ongoing area of research. Currently, the majority of therapeutics targeting translational control are focused on blocking translation initiation through inhibition of eIF4E hyperactivity. However, it will be important to determine whether combined inhibition of ribosome biogenesis, translation initiation, and translation elongation can demonstrate improved therapeutic efficacy in tumours driven by oncogenic AKT.

Indexed as

Cell Transformation, NeoplasticTranscriptional ActivationHumansPeptide Chain Elongation, TranslationalPeptide Chain Initiation, TranslationalProto-Oncogene Proteins c-aktRibosomesProto-Oncogene Proteins c-akt

Identifiers

PMID21772331
PMCPMC3172900
OpenAlexW2040599763

What OpenQuestion 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 OpenQuestion graph.