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Genetic alterations of chromosome 8 genes in oral cancer

Zachary Wei Ern Yong1, Zuraiza Mohamad Zaini1, Thomas George Kallarakkal1

  • 11] Department of Oro-Maxillofacial Surgical and Medical Sciences, Faculty of Dentistry, University of Malaya, Kuala Lumpur, Malaysia [2] Oral Cancer Research &Coordinating Centre (OCRCC), Faculty of Dentistry, University of Malaya, Kuala Lumpur, Malaysia.

Scientific Reports
|August 16, 2014
PubMed

Insights

DNA copy number alterations in chromosome 8 are relevant in oral cancers. EIF3E gene amplification is linked to oral cancer development in non-betel quid chewers.

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Oral squamous cell carcinoma (OSCC) is a significant global health concern.
  • Understanding the genetic underpinnings of OSCC is crucial for developing targeted therapies.
  • Chromosome 8 harbors genes potentially involved in oral cancer development.

Purpose of the Study:

  • To investigate the clinical relevance of DNA copy number alterations (CNAs) on chromosome 8 in oral cancers.
  • To identify specific genes amplified or deleted in OSCC and correlate these with clinical parameters.
  • To explore the potential role of EIF3E gene amplification in OSCC carcinogenesis.

Main Methods:

  • Utilized multiplex ligation-dependent probe amplification (MLPA) to detect copy numbers of 30 selected genes on chromosome 8.
  • Analyzed DNA from 33 patients diagnosed with oral squamous cell carcinoma.
  • Correlated gene copy number alterations with clinical data, including alcohol consumption, betel quid chewing habits, lymph node status, and survival.

Main Results:

  • Gene amplifications were observed, with EIF3E (27.3%), MYC (18.2%), RECQL4 (15.2%), and MYBL1 (12.1%) being the most frequent.
  • Frequent gene losses included GATA4 (24.2%), FGFR1 (24.2%), MSRA (21.2%), and CSGALNACT1 (12.1%).
  • Co-amplification of EIF3E and RECQL4 associated with alcohol consumption; EIF3E amplification linked to non-betel quid chewers and negative lymph node status, but not survival.

Conclusions:

  • EIF3E gene amplification may play a role in the carcinogenesis of OSCC, particularly in individuals who do not chew betel quid.
  • Specific CNAs on chromosome 8, such as EIF3E amplification, are frequent in OSCC and correlate with certain risk factors and clinical features.
  • Further research is warranted to elucidate the precise mechanisms by which EIF3E contributes to oral cancer development.

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