Evidence map›Paper›PMID 30197175›Full record

ReviewTrends in molecular medicine2018

Cancer-Associated PIK3CA Mutations in Overgrowth Disorders.

Ralitsa R Madsen, Bart Vanhaesebroeck, Robert K Semple

Open access · hybridAbstract readReview
In one paragraph

Review in Trends in molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed
19.2field-weighted citation impact, top 1% 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

151 citing papers in PubMed, 272 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  18. Effects of PIK3CA Gene Modifications on Radiosensitivity in Colorectal Cancer Cells.Asian Pacific journal of cancer prevention : APJCP · 2025
    Article
  19. Review
  20. Article

91 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 2 institutions in 1 country.

Ralitsa R MadsenMetabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, University of Cambridge, Cambridge CB2 0QQ, UK; The National Institute for Health Research Cambridge Biomedical Research Centre, Cambridge CB2 0QQ, UK.
Bart VanhaesebroeckUCL Cancer Institute, Paul O'Gorman Building, University College London, London WC1E 6DD, UK.
Robert K SempleMetabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, University of Cambridge, Cambridge CB2 0QQ, UK; The National Institute for Health Research Cambridge Biomedical Research Centre, Cambridge CB2 0QQ, UK; Centre for Cardiovascular Sciences, Queens Medical Research Institute, University of Edinburgh, Little France Crescent, Edinburgh EH16 4TJ, UK. Electronic address: rsemple@exseed.ed.ac.uk.
University of Cambridge · GBCRUK Lung Cancer Centre of Excellence · GB

Funding

Cancer Research UK 15965Cancer Research UK 25722Cancer Research UK C23338/A15965Department of HealthWellcome TrustWellcome Trust 105371/Z/14/ZWellcome Trust 210752/Z/18/Z
6 · The paper itself

Abstract

PIK3CA is one of the most commonly mutated genes in solid cancers. PIK3CA mutations are also found in benign overgrowth syndromes, collectively known as PIK3CA-related overgrowth spectrum (PROS). As in cancer, PIK3CA mutations in PROS arise postzygotically, but unlike in cancer, these mutations arise during embryonic development, with their timing and location critically influencing the resulting disease phenotype. Recent evidence indicates that phosphoinositide 3-kinase (PI3K) pathway inhibitors undergoing trials in cancer can provide a therapy for PROS. Conversely, PROS highlights gaps in our understanding of PI3K's role during embryogenesis and in cancer development. Here, we summarize current knowledge of PROS, evaluate challenges and strategies for disease modeling, and consider the implications of PROS as a paradigm for understanding activating PIK3CA mutations in human development and cancer.

Indexed as

Gene Expression Regulation, NeoplasticMutationCarcinogenesisCell MovementCell ProliferationClass I Phosphatidylinositol 3-KinasesEmbryo, MammalianEmbryonic DevelopmentGenetic Association StudiesGrowth DisordersHumansNeoplasmsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktSignal TransductionClass I Phosphatidylinositol 3-KinasesPIK3CA protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins c-aktcancerovergrowth syndromesPI3KPIK3CA

Identifiers

PMID30197175
PMCPMC6185869
OpenAlexW2889851758

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.