ArticleMolecular cancer therapeutics2012
The association of PI3 kinase signaling and chemoresistance in advanced ovarian cancer.
Article in Molecular cancer therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 97 citations in OpenAlex.
- Trial
- Ascites analysis by a microfluidic chip allows tumor-cell profiling.Proceedings of the National Academy of Sciences of the United States of America · 2013Trial
- Signaling networks and MiRNA crosstalk in ovarian cancer chemoresistance.Journal of ovarian research · 2025Review
- Circulating extracellular vesicles protein expression for early prediction of platinum-resistance in high-grade serous ovarian cancer.Oncogene · 2025Article
- KLF4 promotes cisplatin resistance by activating mTORC1 signaling in ovarian cancer.Discover oncology · 2024Article
- Molecular changes driving low-grade serous ovarian cancer and implications for treatment.International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2024Review
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- Review
- Potential prognostic role of somatic mutations in a set of cancer susceptibility genes in ovarian carcinoma: A follow-up multicentric study from Pakistan.Cancer biomarkers : section A of Disease markers · 2023Article
- Integrated molecular profiling of patient-derived ovarian cancer models identifies clinically relevant signatures and tumor vulnerabilities.International journal of cancer · 2022Article
- Individualized Prediction of Drug Response and Rational Combination Therapy in NSCLC Using Artificial Intelligence-Enabled Studies of Acute Phosphoproteomic Changes.Molecular cancer therapeutics · 2022Article
- PI3K Inhibitors in Advanced Breast Cancer: The Past, The Present, New Challenges and Future Perspectives.Cancers · 2022Review
- A phospho-proteomic study of cetuximab resistance in KRAS/NRAS/BRAFCellular oncology (Dordrecht, Netherlands) · 2021Article
- Article
- A complete map of the Calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) signaling pathway.Journal of cell communication and signaling · 2021Article
- The multi-target small-molecule inhibitor SB747651A shows in vitro and in vivo anticancer efficacy in glioblastomas.Scientific reports · 2021Article
- PRKAR1B-AS2 Long Noncoding RNA Promotes Tumorigenesis, Survival, and Chemoresistance via the PI3K/AKT/mTOR Pathway.International journal of molecular sciences · 2021Article
- Targeting the PI3K/AKT/mTOR pathway in epithelial ovarian cancer, therapeutic treatment options for platinum-resistant ovarian cancer.Cancer drug resistance (Alhambra, Calif.) · 2021Review
- Pharmacological Inhibition of BAD Ser99 Phosphorylation Enhances the Efficacy of Cisplatin in Ovarian Cancer by Inhibition of Cancer Stem Cell-like Behavior.ACS pharmacology & translational science · 2020Article
- Targeting the PI3K/AKT/mTOR/NFκB Axis in Ovarian Cancer.Journal of cellular immunology · 2020Article
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
Evidence that the phosphoinositide 3-kinase (PI3K) pathway is deregulated in ovarian cancer is largely based on the analysis of surgical specimens sampled at diagnosis and may not reflect the biology of advanced ovarian cancer. We aimed to investigate PI3K signaling in cancer cells isolated from patients with advanced ovarian cancer. Ascites samples were analyzed from 88 patients, of whom 61 received further treatment. Cancer cells were immunomagnetically separated from ascites, and the signaling output of the PI3K pathway was studied by quantifying p-AKT, p-p70S6K, and p-GSK3β by ELISA. Relevant oncogenes, such as PIK3CA and AKT, were sequenced by PCR-amplified mass spectroscopy detection methods. In addition, PIK3CA and AKT2 amplifications and PTEN deletions were analyzed by FISH. p-p70S6K levels were significantly higher in cells from 37 of 61 patients who did not respond to subsequent chemotherapy (0.7184 vs. 0.3496; P = 0.0100), and this difference was greater in patients who had not received previous chemotherapy. PIK3CA and AKT mutations were present in 5% and 0% of samples, respectively. Amplification of PIK3CA and AKT2 and deletion of PTEN was seen in 10%, 10%, and 27% of samples, respectively. Mutations of PIK3CA and amplification of PIK3CA/AKT2 or deletion of PTEN did not correlate with levels of p-AKT, p-p70S6K, and p-GSK3β. In patients with advanced ovarian cancer, there is an association between levels of p-p70S6K and response to subsequent chemotherapy. There is no clear evidence that this is driven specifically by PIK3CA or AKT mutations or by amplifications or deletion of PTEN.
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