ArticlePloS one2013
Multiple genetic alterations within the PI3K pathway are responsible for AKT activation in patients with ovarian carcinoma.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 40 citations in OpenAlex.
- Use of comprehensive genomic profiling to direct point-of-care management of patients with gynecologic cancers.Gynecologic oncology · 2016Trial
- CORO1C Regulates the Malignant Biological Behavior of Ovarian Cancer Cells and Modulates the mRNA Expression Profile through the PI3K/AKT Signaling Pathway.Cell biochemistry and biophysics · 2025Article
- NAC1/ACOX2 Axis as a Novel Therapeutic Target for Endometriosis-Related Ovarian Neoplasms.International journal of molecular sciences · 2025Article
- High Frequency ofCancers · 2025Article
- Deciphering the ghost proteome in ovarian cancer cells by deep proteogenomic characterization.Cell death & disease · 2024Article
- Role of Akt/Protein Kinase B in Cancer Metastasis.Biomedicines · 2023Review
- An Immunohistochemical Study of the PTEN/AKT Pathway Involvement in Canine and Feline Mammary Tumors.Animals : an open access journal from MDPI · 2021Article
- Association of Inflammation-Related Gene Polymorphisms With Susceptibility and Radiotherapy Sensitivity in Head and Neck Squamous Cell Carcinoma Patients in Northeast China.Frontiers in oncology · 2021Article
- AKT1 Polymorphism (rs10138227) and Risk of Colorectal Cancer in Moroccan Population: A Case Control Study.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- PI3K/AKT pathway as a key link modulates the multidrug resistance of cancers.Cell death & disease · 2020Review
- Results of an abbreviated phase II study of AKT inhibitor MK-2206 in the treatment of recurrent platinum-resistant high grade serous ovarian, fallopian tube, or primary peritoneal carcinoma (NCT 01283035).Gynecologic oncology reports · 2020Article
- Differential expression of mTOR components in endometriosis and ovarian cancer: Effects of rapalogues and dual kinase inhibitors on mTORC1 and mTORC2 stoichiometry.International journal of molecular medicine · 2019Article
- Akt activation by CaThe Journal of biological chemistry · 2017Article
- Article
- Exome sequencing of lymphomas from three dog breeds reveals somatic mutation patterns reflecting genetic background.Genome research · 2015Article
- Risk prediction model for epithelial ovarian cancer using molecular markers and clinical characteristics.Journal of ovarian research · 2015Article
- RY-2f, an isoflavone analog, overcomes cisplatin resistance to inhibit ovarian tumorigenesis via targeting the PI3K/AKT/mTOR signaling pathway.Oncotarget · 2015Article
- Combined comparative genomic hybridization and transcriptomic analyses of ovarian granulosa cell tumors point to novel candidate driver genes.BMC cancer · 2015Article
- Loss of serum and glucocorticoid-regulated kinase 3 (SGK3) does not affect proliferation and survival of multiple myeloma cell lines.PloS one · 2015Article
- Association of MTOR and AKT Gene Polymorphisms with Susceptibility and Survival of Gastric Cancer.PloS one · 2015Article
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13 authors at 4 institutions in 1 country.
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Abstract
The phosphatidylinositol 3-kinase (PI3K)/AKT pathway is activated in multiple cancers including ovarian carcinoma (OC). However, the relative contribution of the single components within the PI3K pathway to AKT activation in OC is still unclear. We examined 98 tumor samples from Italian OC patients for alterations in the members of the PI3K pathway. We report that AKT is significantly hyperactive in OC compared to normal tissue (n = 93; p<0.0001) and that AKT activation is preferentially observed in the elderly (>58 years old; n = 93; p<0.05). The most frequent alteration is the overexpression of the p110α catalytic subunit of PI3K (63/93, ∼68%); less frequent alterations comprise the loss of PTEN (24/89, 27%) and the overexpression of AKT1 (18/96, 19%) or AKT2 (11/88,12.5%). Mutations in the PIK3CA or KRAS genes were detected at lower frequency (12% and 10%, respectively) whereas mutations in AKT1 or AKT2 genes were absent. Although many tumors presented a single lesion (28/93, of which 23 overexpressed PIK3CA, 1 overexpressed AKT and 4 had lost PTEN), many OC (35/93) presented multiple alterations within the PI3K pathway. Apparently, aberrant PI3K signalling was mediated by activation of the canonical downstream AKT-dependent mTOR/S6K1/4EBP1 pathway and by regulation of expression of oncogenic transcription factors that include HMGA1, JUN-B, FOS and MYC but not by AKT-independent activation of SGK3. FISH analysis indicated that gene amplification of PIK3CA, AKT1 and AKT2 (but not of PI3KR1) and the loss of PTEN are common and may account for changes in the expression of the corresponding proteins. In conclusion, our results indicate that p110α overexpression represents the most frequent alteration within the PI3K/AKT pathway in OC. However, p110α overexpression may not be sufficient to activate AKT signalling and drive ovarian tumorigenesis since many tumors overexpressing PI3K presented at least one additional alteration.
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