Exome and genome sequencing of nasopharynx cancer identifies NF-κB pathway activating mutations

نویسندگان

  • Yvonne Y Li
  • Grace T Y Chung
  • Vivian W Y Lui
  • Ka-Fai To
  • Brigette B Y Ma
  • Chit Chow
  • John K S Woo
  • Kevin Y Yip
  • Jeongsun Seo
  • Edwin P Hui
  • Michael K F Mak
  • Maria Rusan
  • Nicole G Chau
  • Yvonne Y Y Or
  • Marcus H N Law
  • Peggy P Y Law
  • Zoey W Y Liu
  • Hoi-Lam Ngan
  • Pok-Man Hau
  • Krista R Verhoeft
  • Peony H Y Poon
  • Seong-Keun Yoo
  • Jong-Yeon Shin
  • Sau-Dan Lee
  • Samantha W M Lun
  • Lin Jia
  • Anthony W H Chan
  • Jason Y K Chan
  • Paul B S Lai
  • Choi-Yi Fung
  • Suet-Ting Hung
  • Lin Wang
  • Ann Margaret V Chang
  • Simion I Chiosea
  • Matthew L Hedberg
  • Sai-Wah Tsao
  • Andrew C van Hasselt
  • Anthony T C Chan
  • Jennifer R Grandis
  • Peter S Hammerman
  • Kwok-Wai Lo
چکیده

Nasopharyngeal carcinoma (NPC) is an aggressive head and neck cancer characterized by Epstein-Barr virus (EBV) infection and dense lymphocyte infiltration. The scarcity of NPC genomic data hinders the understanding of NPC biology, disease progression and rational therapy design. Here we performed whole-exome sequencing (WES) on 111 micro-dissected EBV-positive NPCs, with 15 cases subjected to further whole-genome sequencing (WGS), to determine its mutational landscape. We identified enrichment for genomic aberrations of multiple negative regulators of the NF-κB pathway, including CYLD, TRAF3, NFKBIA and NLRC5, in a total of 41% of cases. Functional analysis confirmed inactivating CYLD mutations as drivers for NPC cell growth. The EBV oncoprotein latent membrane protein 1 (LMP1) functions to constitutively activate NF-κB signalling, and we observed mutual exclusivity among tumours with somatic NF-κB pathway aberrations and LMP1-overexpression, suggesting that NF-κB activation is selected for by both somatic and viral events during NPC pathogenesis.

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عنوان ژورنال:

دوره 8  شماره 

صفحات  -

تاریخ انتشار 2017