ArticleBritish journal of cancer2013
Targeting EGFR and PI3K pathways in ovarian cancer.
Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Epidermal growth factor receptor blockers for the treatment of ovarian cancer.The Cochrane database of systematic reviews · 2018Pooled it
- Oncogenic EGFR Signaling as a Central Regulator of Chemoresistance in Ovarian Cancer: A Mechanistic Review.International journal of molecular sciences · 2026Review
- A Multiomics and Bioinformatics Analysis of the Role and Mechanism ofInternational journal of genomics · 2026Article
- Article
- EGFR amplification and PI3K pathway mutations identify a subset of breast cancers that synergistically respond to EGFR and PI3K inhibition.bioRxiv : the preprint server for biology · 2025Article
- Elevated SLC4A11 expression promotes OV progression via interaction with EGFR.Scientific reports · 2025Article
- Novel Natural Inhibitors for Glioblastoma by Targeting Epidermal Growth Factor Receptor and Phosphoinositide 3-kinase.Current medicinal chemistry · 2024Article
- Biomarkers expression among paired serous ovarian cancer primary lesions and their peritoneal cavity metastases in treatment-naïve patients: A single-center study.Cancer medicine · 2022Article
- Identification ofOncology letters · 2021Article
- p85β alters response to EGFR inhibitor in ovarian cancer through p38 MAPK-mediated regulation of DNA repair.Neoplasia (New York, N.Y.) · 2021Article
- Bioinformatics Study of Sea Cucumber Peptides as Antibreast Cancer Through Inhibiting the Activity of Overexpressed Protein (EGFR, PI3K, AKT1, and CDK4).Cancer informatics · 2021Article
- Cardiomyopathies and Arrhythmias Induced by Cancer Therapies.Biomedicines · 2020Review
- LPAR1 regulates the development of intratumoral heterogeneity in ovarian serous cystadenocarcinoma by activating the PI3K/AKT signaling pathway.Cancer cell international · 2019Article
- Small Molecules Identified from a Quantitative Drug Combinational Screen Resensitize Cisplatin's Response in Drug-Resistant Ovarian Cancer Cells.Translational oncology · 2018Article
- Dioscin suppresses the viability of ovarian cancer cells by regulating the VEGFR2 and PI3K/AKT/MAPK signaling pathways.Oncology letters · 2018Article
- Therapeutic Targeting of AXL Receptor Tyrosine Kinase Inhibits Tumor Growth and Intraperitoneal Metastasis in Ovarian Cancer Models.Molecular therapy. Nucleic acids · 2017Article
- Systems analysis of apoptotic priming in ovarian cancer identifies vulnerabilities and predictors of drug response.Nature communications · 2017Article
- A loop of cancer-stroma-cancer interaction promotes peritoneal metastasis of ovarian cancer via TNFα-TGFα-EGFR.Oncogene · 2017Article
- Dasatinib + Gefitinib, a non platinum-based combination with enhanced growth inhibitory, anti-migratory and anti-invasive potency against human ovarian cancer cells.Journal of ovarian research · 2017Article
- Ectodomain shedding of the cell adhesion molecule Nectin-4 in ovarian cancer is mediated by ADAM10 and ADAM17.The Journal of biological chemistry · 2017Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe epidermal growth factor receptor (EGFR) is expressed in ovarian cancer, but agents targeting this pathway have shown little effect as single agents. This may be due to the presence of alternative pathways, particularly activation of the PI3K/Akt/MTOR pathway.
methodsWe have therefore examined the effect of inhibitors of this pathway (ZSTK474 and sirolimus) in combination with the EGFR inhibitors erlotinib and gefitinib in ovarian cancer primary cell cultures.
resultsThe single-agent EGFR inhibitors showed little activity, although some activity was seen with the single-agent PI3K inhibitor, ZSTK474. Combinations of ZSTK474 with EGFR inhibitors showed enhanced activity with some evidence of synergy, whereas sirolimus combinations were less active. The results were not explicable on the basis of PIK3CA mutation or amplification, or PTEN loss, although one tumour with a KRAS mutation showed resistance to EGFR inhibitors. However, there was correlation of the EGFR expression with sensitivity to EGFR and resistance to PI3K active agents, and inverse correlation in the sensitivity of individual tumours to agents active against these pathways, suggesting a mechanism of action for the combination.
conclusionPhase I/II clinical trials with these agents should include further pharmacodynamic endpoints and molecular characterisation to identify patients most likely to benefit from this strategy.
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