Evidence map›Paper›PMID 28860563›Full record

ArticleScientific reports2017

PIK3CA exon9 mutations associate with reduced survival, and are highly concordant between matching primary tumors and metastases in endometrial cancer.

Siv Mjos, Henrica M J Werner, Even Birkeland, Frederik Holst, Anna Berg, Mari K Halle, Ingvild L Tangen, Kanthida Kusonmano, Karen K Mauland, Anne M Oyan and 7 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. International journal of molecular sciences · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Genomic Landscape of ctDNA and Real-World Outcomes in Advanced Endometrial Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  19. Class I Phosphoinositide 3-KinaseInternational journal of molecular sciences · 2018
    Review
  20. 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

17 authors at 3 institutions in 3 countries.

Siv MjosCentre for Cancer Biomarkers, Department of Clinical Science, University of Bergen, Bergen, Norway.
Henrica M J WernerCentre for Cancer Biomarkers, Department of Clinical Science, University of Bergen, Bergen, Norway.
Even BirkelandCentre for Cancer Biomarkers, Department of Clinical Medicine, University of Bergen, Bergen, Norway.
Frederik HolstCentre for Cancer Biomarkers, Department of Clinical Science, University of Bergen, Bergen, Norway.ORCID 0000-0002-5928-2175
Anna BergCentre for Cancer Biomarkers, Department of Clinical Science, University of Bergen, Bergen, Norway.
Mari K HalleCentre for Cancer Biomarkers, Department of Clinical Science, University of Bergen, Bergen, Norway.
Ingvild L TangenCentre for Cancer Biomarkers, Department of Clinical Science, University of Bergen, Bergen, Norway.
Kanthida KusonmanoDepartment of Gynecology and Obstetrics, Haukeland University Hospital, Bergen, Norway.
Karen K MaulandCentre for Cancer Biomarkers, Department of Clinical Science, University of Bergen, Bergen, Norway.
Anne M OyanCentre for Cancer Biomarkers, Department of Clinical Science, University of Bergen, Bergen, Norway.
Karl-Henning KallandCentre for Cancer Biomarkers, Department of Clinical Science, University of Bergen, Bergen, Norway.
Aurélia E LewisDepartment of Molecular Biology, University of Bergen, Bergen, Norway.ORCID 0000-0002-3613-5770
Gordon B MillsDepartment of Systems Biology, University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Camilla KrakstadCentre for Cancer Biomarkers, Department of Clinical Science, University of Bergen, Bergen, Norway.
Jone TrovikCentre for Cancer Biomarkers, Department of Clinical Science, University of Bergen, Bergen, Norway.
Helga B SalvesenCentre for Cancer Biomarkers, Department of Clinical Science, University of Bergen, Bergen, Norway.
Erling A HoivikCentre for Cancer Biomarkers, Department of Clinical Science, University of Bergen, Bergen, Norway. erling.hoivik@uib.no.
Haukeland University Hospital · NOThe University of Texas MD Anderson Cancer Center · USUniversity of Bergen · NO

Funding

Targeting the PI3K Signaling Pathway in Endometrial CarcinomaP50CA098258 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BODURKA, DIANE · 2003 to 2020
$32.0M
NCI NIH HHS P50 CA098258
6 · The paper itself

Abstract

Mutations of the phosphoinositide-3-kinase (PI3K) catalytic subunit alpha gene (PIK3CA) are frequent in endometrial cancer. We sequenced exon9 and exon20 of PIK3CA in 280 primary endometrial cancers to assess the relationship with clinicopathologic variables, patient survival and associations with PIK3CA mRNA and phospho-AKT1 by gene expression and protein data, respectively. While PIK3CA mutations generally had no impact on survival, and were not associated with clinicopathological variables, patients with exon9 charge-changing mutations, providing a positive charge at the substituted amino acid residue, were associated with poor survival (p = 0.018). Furthermore, we characterized PIK3CA mutations in the metastatic setting, including 32 patients with matched primary tumors and metastases, and found a high level of concordance (85.7%; 6 out of 7 patients), suggesting limited heterogeneity. PIK3CA mRNA levels were increased in metastases compared to the primary tumors (p = 0.031), independent of PIK3CA mutation status, which rather associated with reduced PIK3CA mRNA expression. PIK3CA mutated tumors expressed higher p-AKT/AKT protein levels, both within primary (p < 0.001) and metastatic lesion (p = 0.010). Our results support the notion that the PI3K signaling pathway might be activated, both dependent- and independently of PIK3CA mutations, an aspect that should be considered when designing PIK3 pathway targeting strategies in endometrial cancer.

Indexed as

MutationUp-RegulationClass I Phosphatidylinositol 3-KinasesEndometrial NeoplasmsExonsFemaleGene Expression Regulation, NeoplasticHumansMAP Kinase Signaling SystemNeoplasm MetastasisPhosphorylationProto-Oncogene Proteins c-aktSequence Analysis, DNASurvival AnalysisAKT1 protein, humanClass I Phosphatidylinositol 3-KinasesPIK3CA protein, humanProto-Oncogene Proteins c-akt

Identifiers

PMID28860563
PMCPMC5578954
OpenAlexW2746256337

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.