ReviewOncogene2008
Class I PI3K in oncogenic cellular transformation.
Review in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 311 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
311 citing papers in PubMed, 591 citations in OpenAlex.
- Article
- Single-Cell Analysis Reveals STARD10 as a Fatty Acid Metabolism Regulator of Breast Cancer Progression via the PI3K/Akt Pathway.International journal of molecular sciences · 2026Article
- Understanding the structural stability and plasticity of VPS34 protein determined by selective/nonselective inhibitors: insights from molecular dynamics simulations.Molecular diversity · 2026Article
- Article
- Monotherapy cancer drug-blind response prediction is limited to intraclass generalization.PLoS computational biology · 2026Article
- Navigating chemoresistance in triple-negative breast cancer: interplay between molecular signalling pathways and immune microenvironment.Molecular biology reports · 2026Review
- Aging, dauer, and stature phenotypes are conferred by structure-directed missense mutations in the endogenous AGE-1/phosphatidylinositol 3-kinase catalytic subunit.bioRxiv : the preprint server for biology · 2026Article
- Signaling pathways and potential therapeutic agents in trastuzumab-induced cardiotoxicity.Apoptosis : an international journal on programmed cell death · 2026Review
- Selective phosphoinositide 3-kinase inhibitors and implication in diabetic retinopathy as pharmacological tools.Frontiers in pharmacology · 2026Review
- Review of ctDNA in breast cancer - present utility and future perspectives.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2026Review
- BEX2 regulates autophagy by inhibiting PIK3CA-p85 interaction in non-small-cell lung cancer cells.Cell communication and signaling : CCS · 2025Article
- Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5.Cancer research communications · 2025Article
- MAPK, PI3K/Akt Pathways, and GSK-3β Activity in Severe Acute Heart Failure in Intensive Care Patients: An Updated Review.Journal of cardiovascular development and disease · 2025Review
- Mechanisms of cisplatin sensitivity and resistance in testicular germ cell tumors and potential therapeutic agents (Review).Experimental and therapeutic medicine · 2025Review
- Targeting on the PI3K/mTOR: a potential treatment strategy for clear cell ovarian carcinoma.Cancer chemotherapy and pharmacology · 2025Article
- Structural insights into isoform-specific RAS-PI3Kα interactions and the role of RAS in PI3Kα activation.Nature communications · 2025Article
- The potential role of rutin, a flavonoid, in the management of cancer through modulation of cell signaling pathways.Open life sciences · 2025Review
- Evaluation of Methylation and Changes in the Transcriptomics and Proteomics of the GRHL3, PHLDA3, and in Patients with Head and Neck Squamous Cell Carcinoma.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2025Article
- Anticancer Drug Discovery from Natural Compounds Targeting PI3K/AKT/mTOR Signaling Pathway.Current medicinal chemistry · 2025Review
- Molecular Basis of Oncogenic PI3K Proteins.Cancers · 2024Review
251 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Class I phosphoinositide 3-kinase (PI3K) is a dimeric enzyme, consisting of a catalytic and a regulatory subunit. The catalytic subunit occurs in four isoforms designated as p110 alpha, p110 beta, p110 gamma and p110 delta. These isoforms combine with several regulatory subunits; for p110 alpha, beta and delta, the standard regulatory subunit is p85, for p110 gamma, it is p101. PI3Ks play important roles in human cancer. PIK3CA, the gene encoding p110 alpha, is mutated frequently in common cancers, including carcinoma of the breast, prostate, colon and endometrium. Eighty percent of these mutations are represented by one of the three amino-acid substitutions in the helical or kinase domains of the enzyme. The mutant p110 alpha shows a gain of function in enzymatic and signaling activity and is oncogenic in cell culture and in animal model systems. Structural and genetic data suggest that the mutations affect regulatory inter- and intramolecular interactions and support the conclusion that there are at least two molecular mechanisms for the gain of function in p110 alpha. One of these mechanisms operates largely independently of binding to p85, the other abolishes the requirement for an interaction with Ras. The non-alpha isoforms of p110 do not show cancer-specific mutations. However, they are often differentially expressed in cancer and, in contrast to p110 alpha, wild-type non-alpha isoforms of p110 are oncogenic when overexpressed in cell culture. The isoforms of p110 have become promising drug targets. Isoform-selective inhibitors have been identified. Inhibitors that target exclusively the cancer-specific mutants of p110 alpha constitute an important goal and challenge for current drug development.
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What OpenQuestion holds
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.