Increased Expression of Phosphatidylinositol 3-Kinase p110[alpha] and Gene Amplification of PIK3CA in Nasopharyngeal Carcinoma

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From: Pathology & Oncology Research(Vol. 22, Issue 2)
Publisher: Springer
Document Type: Report
Length: 305 words

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To access, purchase, authenticate, or subscribe to the full-text of this article, please visit this link: Byline: Wai Kien Yip (1), Pei Yuan He (1,4), Maizaton Atmadini Abdullah (1), Suryati Yusoff (2), Heng Fong Seow (1,3) Keywords: PIK3CA; Akt; Nasopharyngeal carcinoma; Immunohistochemistry Abstract: Molecular alterations in PIK3CA oncogene that encodes the p110[alpha] catalytic subunit of phosphatidylinositol 3-kinase (PI3K p110[alpha]) are commonly found in human cancers. In this study, we examined the expression of PI3K p110[alpha] and PIK3CA gene amplification in 74 nasopharyngeal carcinoma (NPC) cases. Immunohistochemical staining demonstrated overexpression of PI3K p110[alpha] 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 p110[alpha] expression level was correlated with increased PIK3CA copy number (Spearman's rho =0.324, P = 0.02). PI3K p110[alpha] expression and PIK3CA copy number did not associate with Akt phosphorylation, and patient and tumor variables. This study suggests that PI3K p110[alpha] 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. Author Affiliation: (1) Department of Pathology, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia (2) Department of Pathology, Hospital Kuala Lumpur, Kuala Lumpur, Malaysia (3) Institute of Bioscience, Universiti Putra Malaysia, Selangor, Malaysia (4) Department of Gastroenterology, Affiliated Hospital of Chengde Medical University, Chengde, Hebei, China Article History: Registration Date: 04/11/2015 Received Date: 12/03/2015 Accepted Date: 04/11/2015 Online Date: 18/11/2015

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Gale Document Number: GALE|A446641758