ArticleOncogenesis2015
PIK3CA mutations can initiate pancreatic tumorigenesis and are targetable with PI3K inhibitors.
Article in Oncogenesis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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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.
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Who cites it
60 citing papers in PubMed, 73 citations in OpenAlex.
- PI3K/AKT signaling pathway: molecular crossroads in tumorigenesis and therapeutic innovation.Signal transduction and targeted therapy · 2026Review
- Molecular Imaging in Pancreatic Cancer: Current Applications and Future Perspectives.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Precision Medicine in Pancreatic Cancer: Targeting KRAS and Beyond.Targeted oncology · 2026Review
- An integrative mutational and network analysis of pancreatic cancer reveals key genes, and signalling pathways.Functional & integrative genomics · 2026Article
- Loss of PIK3CA AllowsCells · 2026Article
- Loss of PIK3CA allowsbioRxiv : the preprint server for biology · 2026Article
- Commentary: GETgene-AI: a framework for prioritizing actionable cancer drug targets.Frontiers in systems biology · 2026Article
- Tissue-based genomic profiling of 300,000 tumors highlights the detection of variants with low allele fraction.NPJ precision oncology · 2025Article
- Diagnostic insights into solid pseudopapillary neoplasms of the pancreas: a decade of experience with pediatric representation.Diagnostic pathology · 2025Article
- Mechanistic insights and therapeutic strategies for targeting autophagy in pancreatic ductal adenocarcinoma.Discover oncology · 2025Review
- Comprehensive molecular analysis of 26 newly established human pancreatic ductal adenocarcinoma cell lines reveals two clusters with variating drug sensitivities.Cancer cell international · 2025Article
- Article
- Functionalized Nanomaterials In Pancreatic Cancer Theranostics And Molecular Imaging.ChemistryOpen · 2025Review
- GETgene-AI: a framework for prioritizing actionable cancer drug targets.Frontiers in systems biology · 2025Article
- Development of a novel PIK3CA-mutated pancreatic tumor mouse model and evaluation of the therapeutic effects of a PI3K inhibitor.PloS one · 2025Article
- Construction and validation of immunogenic cell death-related molecular clusters, signature, and immune landscape in pancreatic cancer.Clinical and experimental medicine · 2024Article
- MRTX1133's promise for treating KRASJournal of gastrointestinal oncology · 2024Article
- Clinical practice recommendations for the use of next-generation sequencing in patients with solid cancer: a joint report from KSMO and KSP.Journal of pathology and translational medicine · 2024Review
- Clinical Practice Recommendations for the Use of Next-Generation Sequencing in Patients with Solid Cancer: A Joint Report from KSMO and KSP.Cancer research and treatment · 2024Review
- Deciphering cellular plasticity in pancreatic cancer for effective treatments.Cancer metastasis reviews · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Aberrations in the phosphoinositide 3-kinase (PI3K) signaling pathway have a key role in the pathogenesis of numerous cancers by altering cell growth, metabolism, proliferation and apoptosis. Interest in targeting the PI3K signaling cascade continues, as new agents are being clinically evaluated. PIK3CA mutations result in a constitutively active PI3K and are present in a subset of pancreatic cancers. Here we examine mutant PIK3CA-mediated pancreatic tumorigenesis and the response of PIK3CA mutant pancreatic cancers to dual PI3K/mammalian target of rapamycin (mTOR) inhibition. Two murine models were generated expressing a constitutively active PI3K within the pancreas. An increase in acinar-to-ductal metaplasia and pancreatic intraepithelial neoplasms (PanINs) was identified. In one model these lesions were detected as early as 10 days of age. Invasive pancreatic ductal adenocarcinoma developed in these mice as early as 20 days of age. These cancers were highly sensitive to treatment with dual PI3K/mTOR inhibition. In the second model, PanINs and invasive cancer develop with a greater latency owing to a lesser degree of PI3K pathway activation in this murine model. In addition to PI3K pathway activation, increased ERK1/2 signaling is common in human pancreatic cancers. Phosphorylation of ERK1/2 was also investigated in these models. Phosphorylation of ERK1/2 is demonstrated in the pre-neoplastic lesions and invasive cancers. This activation of ERK1/2 is diminished with dual PI3K/mTOR inhibition. In summary, PIK3CA mutations can initiate pancreatic tumorigenesis and these cancers are particularly sensitive to dual PI3K/mTOR inhibition. Future studies of PI3K pathway inhibitors for patients with PIK3CA mutant pancreatic cancers are warranted.
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Registered trials
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.