Evidence map›Paper›PMID 22370636›Full record

ArticleOncogene2013

Conditional activation of Pik3ca(H1047R) in a knock-in mouse model promotes mammary tumorigenesis and emergence of mutations.

W Yuan, E Stawiski, V Janakiraman, E Chan, S Durinck, K A Edgar, N M Kljavin, C S Rivers, F Gnad, M Roose-Girma and 11 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

50 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Molecular principles underlying aggressive cancers.Signal transduction and targeted therapy · 2025
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. PI3K Inhibitors in Cancer: Clinical Implications and Adverse Effects.International journal of molecular sciences · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. How to Choose a Mouse Model of Breast Cancer, a Genomic Perspective.Journal of mammary gland biology and neoplasia · 2019
    Review
  17. In situ growth in early lung adenocarcinoma may represent precursor growth or invasive clone outgrowth-a clinically relevant distinction.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2019
    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

21 authors at 1 institution.

W YuanDepartment of Molecular Biology, Genentech Inc., South San Francisco, CA 94080, USA.
E Stawiski
V Janakiraman
E Chan
S Durinck
K A Edgar
N M Kljavin
C S Rivers
F Gnad
M Roose-Girma
P M Haverty
G Fedorowicz
S Heldens
R H Soriano
Z Zhang
J J Wallin
L Johnson
M Merchant
Z Modrusan
H M Stern
S Seshagiri
Genentech

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oncogenic mutations in PIK3CA, which encodes the phosphoinositide-3-kinase (PI3K) catalytic subunit p110α, occur in ∼25% of human breast cancers. In this study, we report the development of a knock-in mouse model for breast cancer where the endogenous Pik3ca allele was modified to allow tissue-specific conditional expression of a frequently found Pik3ca(H1047R) (Pik3ca(e20H1047R)) mutant allele. We found that activation of the latent Pik3ca(H1047R) allele resulted in breast tumors with multiple histological types. Whole-exome analysis of the Pik3ca(H1047R)-driven mammary tumors identified multiple mutations, including Trp53 mutations that appeared spontaneously during the development of adenocarinoma and spindle cell tumors. Further, we used this model to test the efficacy of GDC-0941, a PI3K inhibitor, in clinical development, and showed that the tumors respond to PI3K inhibition.

Indexed as

Gene Knock-In TechniquesMutationAdenocarcinomaAllelesAnimalsBase SequenceClass I Phosphatidylinositol 3-KinasesEnzyme ActivationFemaleGene Expression Regulation, NeoplasticGenomicsHumansMammary Neoplasms, ExperimentalMiceOrgan SpecificityPhosphatidylinositol 3-KinasesClass I Phosphatidylinositol 3-KinasesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPik3ca protein, mouseProtein Kinase InhibitorsTumor Suppressor Protein p53

Identifiers

PMID22370636
PMCPMC3550595
OpenAlexW2050105520

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.