ArticlePloS one2016
Colon Cancer Tumorigenesis Initiated by the H1047R Mutant PI3K.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
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- Multi-ancestral origin of intestinal tumors: Impact on growth, progression, and drug efficacy.Cancer reports (Hoboken, N.J.) · 2022Article
- Role of radical quenching activity of dihydrocanaric acid in the treatment of cancer-experimental and theoretical.3 Biotech · 2020Article
- OncogenicProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Activating Mutations inClinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- MTORC1/2 Inhibition as a Therapeutic Strategy forMolecular cancer therapeutics · 2019Article
- Characterization of an Amphiphilic Phosphonated Calixarene Carrier Loaded With Carboplatin and Paclitaxel: A Preliminary Study to Treat Colon CancerFrontiers in bioengineering and biotechnology · 2019Article
- Cancer-Associated PIK3CA Mutations in Overgrowth Disorders.Trends in molecular medicine · 2018Review
- Resistant starch prevents tumorigenesis of dimethylhydrazine-induced colon tumors via regulation of an ER stress-mediated mitochondrial apoptosis pathway.International journal of molecular medicine · 2018Article
- Downregulation of PIK3CA via antibody-esiRNA-complexes suppresses human xenograft tumor growth.PloS one · 2018Article
- PI3K pathway mutations are associated with longer time to local progression after radioembolization of colorectal liver metastases.Oncotarget · 2017Article
- Molecular Profiles Guide Colorectal Cancer Treatment.Federal practitioner : for the health care professionals of the VA, DoD, and PHS · 2016Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The phosphoinositide 3-kinase (PI3K) signaling pathway is critical for multiple important cellular functions, and is one of the most commonly altered pathways in human cancers. We previously developed a mouse model in which colon cancers were initiated by a dominant active PI3K p110-p85 fusion protein. In that model, well-differentiated mucinous adenocarcinomas developed within the colon and initiated through a non-canonical mechanism that is not dependent on WNT signaling. To assess the potential relevance of PI3K mutations in human cancers, we sought to determine if one of the common mutations in the human disease could also initiate similar colon cancers. Mice were generated expressing the Pik3caH1047R mutation, the analog of one of three human hotspot mutations in this gene. Mice expressing a constitutively active PI3K, as a result of this mutation, develop invasive adenocarcinomas strikingly similar to invasive adenocarcinomas found in human colon cancers. These tumors form without a polypoid intermediary and also lack nuclear CTNNB1 (β-catenin), indicating a non-canonical mechanism of tumor initiation mediated by the PI3K pathway. These cancers are sensitive to dual PI3K/mTOR inhibition indicating dependence on the PI3K pathway. The tumor tissue remaining after treatment demonstrated reduction in cellular proliferation and inhibition of PI3K signaling.
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