Evidence map›Paper›PMID 28532501›Full record

ArticleMolecular cancer2017

PIK3CA hotspot mutations differentially impact responses to MET targeting in MET-driven and non-driven preclinical cancer models.

Lluís Nisa, Pascal Häfliger, Michaela Poliaková, Roland Giger, Paola Francica, Daniel Matthias Aebersold, Roch-Philippe Charles, Yitzhak Zimmer, Michaela Medová

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Understanding the distinct role of PI3K(p110Frontiers in cardiovascular medicine · 2026
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  2. Article
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  6. Article
  7. Review
  8. Article
  9. Review
  10. TargetingCancer discovery · 2020
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. The Role of PI3K in Met Driven Cancer: A Recap.Frontiers in molecular biosciences · 2018
    Review
  16. Article
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

9 authors at 2 institutions in 1 country.

Lluís NisaDepartment of Clinical Research, Inselspital, Bern University Hospital, and University of Bern, 3008, Bern, Switzerland. lluis.nisa@dkf.unibe.ch.
Pascal HäfligerInstitute of Biochemistry and Molecular Medicine, University of Bern, 3012, Bern, Switzerland.
Michaela PoliakováDepartment of Clinical Research, Inselspital, Bern University Hospital, and University of Bern, 3008, Bern, Switzerland.
Roland GigerDepartment of Otorhinolaryngology - Head and Neck Surgery, Inselspital, Bern University Hospital, and University of Bern, 3010, Bern, Switzerland.
Paola FrancicaDepartment of Clinical Research, Inselspital, Bern University Hospital, and University of Bern, 3008, Bern, Switzerland.
Daniel Matthias AebersoldDepartment of Clinical Research, Inselspital, Bern University Hospital, and University of Bern, 3008, Bern, Switzerland.
Roch-Philippe CharlesInstitute of Biochemistry and Molecular Medicine, University of Bern, 3012, Bern, Switzerland.
Yitzhak ZimmerDepartment of Clinical Research, Inselspital, Bern University Hospital, and University of Bern, 3008, Bern, Switzerland.
Michaela MedováDepartment of Clinical Research, Inselspital, Bern University Hospital, and University of Bern, 3008, Bern, Switzerland. michaela.medova@dkf.unibe.ch.
University of Bern · CHUniversity Hospital of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe MET receptor tyrosine kinase represents a promising target in cancer. PIK3CA activating mutations are common in several tumor types and can potentially confer resistance to anti-receptor tyrosine kinase therapy.

methodsMET and/or PI3K pathway inhibition was assessed in NIH3T3 cells harboring MET-activating point mutation with or without ectopic expression of PIK3CA

resultsPIK3CA

conclusionsPIK3CA mutations can lead to resistance to MET inhibition, supporting future clinical evaluation of combinations of PI3K and MET inhibitors in common scenarios of malignant neoplasms featuring aberrant MET expression and PIK3CA mutations.

Indexed as

MutationAnimalsCell Line, TumorCell ProliferationCell SurvivalClass I Phosphatidylinositol 3-KinasesDisease Models, AnimalDrug Resistance, NeoplasmMiceNeoplasmsNIH 3T3 CellsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsProto-Oncogene Proteins c-metTumor BurdenClass I Phosphatidylinositol 3-KinasesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPik3ca protein, mouseProtein Kinase InhibitorsProto-Oncogene Proteins c-metHead and neck cancerMET receptor tyrosine kinasePI3K pathwayPIK3CA mutationsResistance mechanisms

Identifiers

PMID28532501
PMCPMC5441085
OpenAlexW2620079993

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.