Evidence map›Paper›PMID 30406111›Full record

ReviewFrontiers in molecular biosciences2018

The Role of PI3K in Met Driven Cancer: A Recap.

Alexia Hervieu, Stéphanie Kermorgant

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular biosciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. The Landscape ofJTO clinical and research reports · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Targeting MET in Non-Small Cell Lung Cancer (NSCLC): A New Old Story?International journal of molecular sciences · 2023
    Review
  13. Article
  14. Review
  15. Phosphoinositide 3-Kinases as Potential Targets for Thrombosis Prevention.International journal of molecular sciences · 2022
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Updated Insights on EGFR Signaling Pathways in Glioma.International journal of molecular sciences · 2021
    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

2 authors at 1 institution in 1 country.

Alexia HervieuSignal Transduction and Molecular Pharmacology Team, Cancer Therapeutics Division, Institute of Cancer Research, Sutton, United Kingdom.
Stéphanie KermorgantSpatial Signalling Team, Centre for Tumor Biology, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom.
Queen Mary University of London · GB

Funding

Medical Research Council G0501003Medical Research Council MR/R009732/1
6 · The paper itself

Abstract

The Receptor Tyrosine Kinase (RTK) Met, overexpressed or mutated in cancer, plays a major role in cancer progression and represents an attractive target for cancer therapy. However RTK inhibitors can lead to drug resistance, explaining the necessity to develop therapies that target downstream signaling. Phosphatidylinositide 3-kinase (PI3K) is one of the most deregulated pathways in cancer and implicated in various types of cancer. PI3K signaling is also a major signaling pathway downstream of RTK, including Met. PI3K major effectors include Akt and "mechanistic Target of Rapamycin" (mTOR), which each play key roles in numerous and various cell functions. Advancements made due to the development of molecular and pharmaceutical tools now allow us to delve into the roles of each independently. In this review, we summarize the current understanding we possess of the activation and role of PI3K/Akt/mTOR, downstream of Met, in cancer.

Indexed as

AktcancerMetmTORPI3Ksignaling

Identifiers

PMID30406111
PMCPMC6207648
OpenAlexW2898296584

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.