English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

The gene encoding phosphatidylinositol 3-kinase catalytic subunit α-isoform ( PIK3CA ,  p110α ) is frequently activated by mutation in human cancers. Based on detection in some breast cancer precursors,  PIK3CA  mutations have been proposed to have a role in tumor initiation. To investigate this hypothesis, we generated a novel mouse model with a Cre-recombinase regulated allele of  p110α  (myristoylated- p110α,  myr- p110α ) along with  p53   fl/fl   deletion and  Kras   G12D   also regulated by Cre-recombinase. After instillation of adenovirus-expressing Cre-recombinase into mammary ducts, we found that myr- p110α  accelerated breast tumor initiation in a copy number-dependent manner. Breast tumors induced by  p53   fl/fl  ; Kras   G12D   with no or one copy of myr- p110α  had predominantly sarcomatoid features, whereas two copies of myr- p110α  resulted in tumors with a carcinoma phenotype. This novel model provides experimental support for importance of active p110α in breast tumor initiation, and shows that the amount of PI3K activity can affect the rate of tumor initiation and modify the histological phenotype of breast cancer.

Constitutively activated PI3K accelerates tumor initiation and modifies histopathology of breast cancer