ReviewBiochimica et biophysica acta2010
Somatic mutations in PI3Kalpha: structural basis for enzyme activation and drug design.
Review in Biochimica et biophysica acta, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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.
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.
Who cites it
13 citing papers in PubMed.
- A Computational Framework for the Design and Development of Isoform Selective PI3Kα Inhibitors as Novel Anticancer Agents.Molecules (Basel, Switzerland) · 2026Article
- Molecular Basis of Oncogenic PI3K Proteins.Cancers · 2024Review
- Structural and mechanistic insights provided by single particle cryo-EM analysis of phosphoinositide 3-kinase (PI3Kα).Biochimica et biophysica acta. Reviews on cancer · 2023Review
- Structural insights into the interaction of three Y-shaped ligands with PI3Kα.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Cryo-EM structures of cancer-specific helical and kinase domain mutations of PI3Kα.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Nanobodies and chemical cross-links advance the structural and functional analysis of PI3Kα.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Class I PI3K Biology.Current topics in microbiology and immunology · 2022Article
- Combating TKI resistance in CML by inhibiting the PI3K/Akt/mTOR pathway in combination with TKIs: a review.Medical oncology (Northwood, London, England) · 2021Review
- Impact of p85α Alterations in Cancer.Biomolecules · 2019Review
- PIK3CA exon9 mutations associate with reduced survival, and are highly concordant between matching primary tumors and metastases in endometrial cancer.Scientific reports · 2017Article
- Oncogenic mutations weaken the interactions that stabilize the p110α-p85α heterodimer in phosphatidylinositol 3-kinase α.The FEBS journal · 2015Article
- Activation of PI3Kα by physiological effectors and by oncogenic mutations: structural and dynamic effects.Biophysical reviews · 2014Article
- Capitalizing on tumor genotyping: towards the design of mutation specific inhibitors of phosphoinsitide-3-kinase.Advances in enzyme regulation · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
The PI3K pathway is a communication hub coordinating critical cell functions including cell survival, cell growth, proliferation, motility and metabolism. Because PI3Kalpha harbors recurrent somatic mutations resulting in gains of function in human cancers, it has emerged as an important drug target for many types of solid tumors. Various PI3K isoforms are also being evaluated as potential therapeutic targets for inflammation, heart disease, and hematological malignancies. Structural biology is providing insights into the flexibility of the PI3Ks, and providing basis for understanding the effects of mutations, drug resistance and specificity.
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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.