ReviewBritish journal of cancer2023
The emerging role of PI3K inhibitors for solid tumour treatment and beyond.
Review in British journal of cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 68 citations in OpenAlex.
- PI3K signaling in breast cancer: therapeutic advances versus adaptive resistance.The Journal of clinical investigation · 2026Review
- Targeting the PI3K/Akt Signaling Pathway: A Promising Therapeutic Strategy to Reduce Cancer Mortality and Overcome Chemoresistance.Health science reports · 2026Article
- Molecular architecture responsible for specific inhibition of oncogenic PI3KActa pharmaceutica Sinica. B · 2026Article
- PI3K/AKT signaling pathway: molecular crossroads in tumorigenesis and therapeutic innovation.Signal transduction and targeted therapy · 2026Review
- Contemporary design of small-molecule kinase modulators: orthosteric, allosteric and induced-proximity strategies.Nature reviews. Drug discovery · 2026Review
- Identification of novel PI3Kα inhibitors for colon cancer treatment via virtual screening, molecular dynamics simulation, and in vitro activity validation.Molecular diversity · 2026Article
- Primary Neuroendocrine Carcinoma of the Breast: A Diagnostic Challenge and Case Report.Cancer reports (Hoboken, N.J.) · 2026Article
- Optimizing anti-PI3Kδ and anti-LAG-3 immunotherapy dosing regimens in a mouse model of triple-negative breast cancer improves outcome by removing treatment-related adverse events.Journal for immunotherapy of cancer · 2026Article
- PI3K/mTOR inhibition attenuates cigarette smoke-induced senescence and SASP in oral fibroblasts: implications for tumor microenvironment remodeling.Frontiers in cell and developmental biology · 2026Article
- Inavolisib-based Combination Therapy for the Treatment of PIK3CAMutated HR+/HER2- Breast Cancer: An Overview.Mini reviews in medicinal chemistry · 2026Review
- Non-small cell lung cancer after EGFR-TKI resistance: from drug resistance mechanisms to precision interventions.Frontiers in pharmacology · 2026Review
- Review
- Kinase signaling cascades: an updated mechanistic landscape.Chemical science · 2025Review
- Drivers of Pancreatic Cancer: Beyond the Big 4.Cancers · 2025Review
- Comprehensive analysis of PIK3CA mutations in advanced colorectal cancer using circulating tumor DNA profiling.NPJ precision oncology · 2025Article
- The interplay between driver mutation and oxidative stress in colorectal cancer: from pathogenesis to therapeutics.Journal of translational medicine · 2025Review
- Therapeutic options for human papillomavirus-positive tonsil and base of tongue cancer.Journal of internal medicine · 2025Review
- Zinc Finger Protein 639 Expression Is a Novel Prognostic Determinant in Breast Cancer.Journal of breast cancer · 2025Article
- Inavolisib: First Approval.Drugs · 2025Review
- Hybridization-based discovery of novel quinazoline-2-indolinone derivatives as potent and selective PI3Kα inhibitors.Journal of advanced research · 2025Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phosphoinositide 3-kinases (PI3Ks) play a central role in tumourigenesis with recurrent activating mutations of its p110α subunit (PIK3CA) identified in several tumours. Although several PI3K inhibitors are approved for haematological malignancies, only alpelisib was approved in solid tumours and for the treatment of PIK3CA-related overgrowth spectrum (PROS) syndrome. Traditional PI3K inhibitors inhibit both wild-type and mutant PI3K with almost equal potency, thus limiting their efficacy due to on-target toxicity. Since the initiation of phase I clinical trials investigating next generation allosteric mutant and isoform selective PIK3CA inhibitors, there has been a surge in interest in PIK3CA targeting in solid tumours. Preclinical characterisation of these compounds showed that maximal mutant protein inhibition fails to elicit metabolic and glucose homoeostasis dysregulation, one of the dose limiting toxicities of both selective and pan PI3K inhibitors. While extreme selectivity can be hypothesised to grant activity and safety advantage to these novel agents, on the other hand reduced benefit can be speculated for patients harbouring multiple or rare PIK3CA mutations. This review summarises the current understanding of PI3K alterations and the state-of-the-art treatment strategies in PI3K driven solid tumours, while also exploring the potential intrinsic and acquired resistance mechanisms to these agents, and the emerging role of mutant selective PIK3CA inhibitors.
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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.