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Differences in cancer gene copy number alterations between Epstein‐Barr virus‐positive and Epstein‐Barr virus‐negative nasopharyngeal carcinoma
Author(s) -
Ooft Marc Lucas,
van Ipenburg Jolique,
van de Loo Rob J. M.,
de Jong Rick,
Moelans Cathy B.,
de Bree Remco,
de Herdt Martine J.,
Koljenović Senada,
de Jong R. Baatenburg,
Hardillo J.,
Willems Stefan Martin
Publication year - 2018
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/hed.25195
Subject(s) - nasopharyngeal carcinoma , epstein–barr virus , biology , gene duplication , cancer , carcinogenesis , virus , gene , cancer research , virology , medicine , genetics , radiation therapy
Background Nasopharyngeal carcinoma (NPC) treatment is mainly based on clinical staging. We hypothesize that better understanding of the molecular heterogeneity of NPC can aid in better treatment decisions. Therefore, the purpose of this study was to present our exploration of cancer gene copy‐number alterations (CNAs) of Epstein‐Barr virus (EBV)‐positive and EBV‐negative NPC. Methods Multiplex ligation‐dependent probe amplification was applied to detect CNAs of 36 cancer genes (n = 103). Correlation between CNAs, clinicopathological features, and survival were examined. Results The CNAs occurred significantly more in EBV‐negative NPC, with PIK3CA and MCCC1 ( P < .001) gain/amplification occurring more frequently. Gain/amplification of cyclin‐L1 (CCNL1) and PTK2 ( P < .001) predict worse disease‐free survival (DFS) in EBV‐positive NPC. Conclusion The EBV‐positive and EBV‐negative NPC show some similarities in cancer gene CNAs suggesting a common pathogenic route but also important differences possibly indicating divergence in oncogenesis. Copy number gain/amplification of CCNL1 and PTK2 are possibly good predictors of survival in EBV‐positive NPC.