ArticleProteins2009
PIK3CA somatic mutations in breast cancer: Mechanistic insights from Langevin dynamics simulations.
Article in Proteins, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Mapping Mutations and Signaling Network Interactions to Guide Precision Therapy in Gallbladder Cancer.Cancer reports (Hoboken, N.J.) · 2026Review
- HLA class II-restricted T cell epitopes in public neoantigens of ESR1 and PIK3CA in breast cancer.BMC cancer · 2025Article
- PIK3CA mutations in breast cancer: A Tunisian series.PloS one · 2023Article
- Chip-based digital Polymerase Chain Reaction as quantitative technique for the detection ofHeliyon · 2022Article
- Article
- The Spectrum, Tendency and Predictive Value ofFrontiers in oncology · 2021Article
- Prevalence of Phosphatidylinositol-3-Kinase (PI3K) Pathway Alterations and Co-alteration of Other Molecular Markers in Breast Cancer.Frontiers in oncology · 2020Article
- Molecular characterisation in tongue squamous cell carcinoma reveals key variants potentially linked to clinical outcomes.Cancer biomarkers : section A of Disease markers · 2020Article
- Helical and kinase domain mutations ofOncology letters · 2019Article
- Rapid detection of genetic mutations in individual breast cancer patients by next-generation DNA sequencing.Human genomics · 2015Article
- Investigating the structure and dynamics of the PIK3CA wild-type and H1047R oncogenic mutant.PLoS computational biology · 2014Article
- A graph theoretic approach to utilizing protein structure to identify non-random somatic mutations.BMC bioinformatics · 2014Article
- Utilizing protein structure to identify non-random somatic mutations.BMC bioinformatics · 2013Article
- Somatic mutations in PI3Kalpha: structural basis for enzyme activation and drug design.Biochimica et biophysica acta · 2010Review
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Somatic mutations in PIK3CA (phosphatidylinositol-3 kinase, catalytic subunit, alpha isoform) are reported in breast and other human cancers to concentrate at hotspots within its kinase and helical domains. Most of these mutations cause kinase gain of function in vitro and are associated with oncogenicity in vivo. However, little is known about the mechanisms driving tumor development. We have performed computational structural studies on a homology model of wildtype PIK3CA plus recurrent H1047R, H1047L, and P539R mutations, located in the kinase and helical domains, respectively. The time evolution of the structures show that H1047R/L mutants exhibit a larger area of the catalytic cleft between the kinase N- and C-lobes compared with the wildtype that could facilitate the entrance of substrates. This larger area might yield enhanced substrate-to-product turnover associated with oncogenicity. In addition, the H1047R/L mutants display increased kinase activation loop mobility, compared with the wildtype. The P539R mutant forms more hydrogen bonds and salt-bridge interactions than the wildtype, properties that are associated with enhanced thermostability. Mutant-specific differences in the catalytic cleft and activation loop behavior suggest that structure-based mutant-specific inhibitors can be designed for PIK3CA-positive breast cancers.
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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.