Evidence map›Paper›PMID 22666336›Full record

ArticlePloS one2012

Physiological levels of Pik3ca(H1047R) mutation in the mouse mammary gland results in ductal hyperplasia and formation of ERα-positive tumors.

Anjali Tikoo, Vincent Roh, Karen G Montgomery, Ivan Ivetac, Paul Waring, Rebecca Pelzer, Lauren Hare, Mark Shackleton, Patrick Humbert, Wayne A Phillips

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. CarcSeq detection of lorcaserin-induced clonal expansion of Pik3ca H1047R mutants in rat mammary tissue.Toxicological sciences : an official journal of the Society of Toxicology · 2024
    Article
  5. Advances in Immunocompetent Mouse and Rat Models.Cold Spring Harbor perspectives in medicine · 2024
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Short-term PI3K Inhibition Prevents Breast Cancer in Preclinical Models.Cancer prevention research (Philadelphia, Pa.) · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Molecular cancer research : MCR · 2020
    Article
  16. Article
  17. Article
  18. OncogenicProceedings of the National Academy of Sciences of the United States of America · 2019
    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

10 authors at 2 institutions in 1 country.

Anjali TikooSurgical Oncology Research Laboratory, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia.
Vincent Roh
Karen G Montgomery
Ivan Ivetac
Paul Waring
Rebecca Pelzer
Lauren Hare
Mark Shackleton
Patrick Humbert
Wayne A Phillips
Peter MacCallum Cancer Centre · AUThe University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PIK3CA, the gene coding for the p110α subunit of phosphoinositide 3-kinase, is frequently mutated in a variety of human tumors including breast cancers. To better understand the role of mutant PIK3CA in the initiation and/or progression of breast cancer, we have generated mice with a conditional knock-in of the common activating mutation, Pik3ca(H1047R), into one allele of the endogenous gene in the mammary gland. These mice developed a ductal anaplasia and hyperplasia by 6 weeks of age characterized by multi-layering of the epithelial lining of the mammary ducts and expansion of the luminal progenitor (Lin(-); CD29(lo); CD24(+); CD61(+)) cell population. The Pik3ca(H1047R) expressing mice eventually develop mammary tumors with 100% penetrance but with a long latency (>12 months). This is significantly longer than has been reported for transgenic models where expression of the mutant Pik3ca is driven by an exogenous promoter. Histological analysis of the tumors formed revealed predominantly ERα-positive fibroadenomas, carcinosarcomas and sarcomas. In vitro induction of Pik3ca(H1047R) in immortalized mammary epithelial cells also resulted in tumor formation when injected into the mammary fat pad of immunodeficient recipient mice. This novel model, which reproduces the scenario of a heterozygous somatic mutation occurring in the endogenous PIK3CA gene, will thus be a valuable tool for investigating the role of Pik3ca(H1047R) mutation in mammary tumorigenesis both in vivo and in vitro.

Indexed as

MutationAllelesAnimalsBase SequenceClass I Phosphatidylinositol 3-KinasesEstrogen Receptor alphaFemaleGene Expression Regulation, DevelopmentalGene Expression Regulation, NeoplasticGene Knock-In TechniquesHyperplasiaMammary Glands, AnimalMammary Neoplasms, ExperimentalMiceMolecular Sequence DataPhosphatidylinositol 3-KinasesClass I Phosphatidylinositol 3-KinasesEstrogen Receptor alphaPhosphatidylinositol 3-KinasesPik3ca protein, mouse

Identifiers

PMID22666336
PMCPMC3364244
OpenAlexW2055808017

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.