ArticlePathology oncology research : POR2016
Increased Expression of Phosphatidylinositol 3-Kinase p110α and Gene Amplification of PIK3CA in Nasopharyngeal Carcinoma.
Article in Pathology oncology research : POR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- In silico prediction of the action of bromelain on PI3K/Akt signalling pathway to arrest nasopharyngeal cancer oncogenesis by targeting phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha protein.BMC research notes · 2024Article
- Article
- Relationship Between PIK3CA Amplification and P110α and CD34 Tissue Expression as Angiogenesis Markers in Iranian Women with Sporadic Breast Cancer.Iranian journal of pathology · 2018Article
- Meta-signature of mutated genes in gallbladder cancer: evidence based high throughput screening assays.Annals of translational medicine · 2016Article
- Serum- and glucocorticoid-inducible kinase 3 is a potential oncogene in nasopharyngeal carcinoma.Brazilian journal of otorhinolaryngologyArticle
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Molecular alterations in PIK3CA oncogene that encodes the p110α catalytic subunit of phosphatidylinositol 3-kinase (PI3K p110α) are commonly found in human cancers. In this study, we examined the expression of PI3K p110α and PIK3CA gene amplification in 74 nasopharyngeal carcinoma (NPC) cases. Immunohistochemical staining demonstrated overexpression of PI3K p110α protein in 44.6% (33/74) of NPCs and 4.8% (2/42) of the adjacent normal nasopharyngeal mucosa. Copy number of PIK3CA gene was successfully analyzed in 51 of the total NPC cases and 19 non-malignant nasopharynx tissues by quantitative real-time PCR. Using mean + 2(standard deviation) of copy numbers in the non-malignant nasopharynx tissues as a cutoff value, PIK3CA copy number gain was found in 10 of 51 (19.6%) NPC cases. High PI3K p110α expression level was correlated with increased PIK3CA copy number (Spearman's rho =0.324, P = 0.02). PI3K p110α expression and PIK3CA copy number did not associate with Akt phosphorylation, and patient and tumor variables. This study suggests that PI3K p110α overexpression, which is attributed, at least in part, to PIK3CA gene amplification, may contribute to NPC pathogenesis. However, these molecular aberrations may not be responsible for activation of Akt signaling in NPC.
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