Published on 06 Jun 2024

Common virus can trigger quicker growth of nasopharyngeal cancer: Study

Associate Professor Melissa Jane Fullwood from NTU’s School of Biological Sciences (SBS) and NTU SBS Research Fellow Dr Ruchi Choudhary, the NTU co-lead authors of the study

Scientists from NTU Singapore and Chiba University in Japan have shown how the Epstein-Barr virus (EBV) alters how specific genes are regulated, making nasopharyngeal cancer tumours (NPC) grow faster.The Epstein-Barr virus, also known as human herpesvirus 4, is one of the most common human viruses, causing infectious mononucleosis, also known as mono or glandular fever, and other illnesses.

Led by Associate Professor Melissa Jane Fullwood, from NTU’s School of Biological Sciences and Professor Atsushi Kaneda from the Graduate School of Medicine, Chiba University, the researchers found that EBV tricks human cells into turning on specific genes that promote cancerous growth. Studying cells from patients with NPC, scientists observed how the virus acts as it infects nasopharynx cells to ‘switch on’ genes that trigger the rapid multiplication of NPC cells.

This new study provides additional insight into the link between EBV and NPC. Although previous research has associated the two diseases, researchers have not convincingly demonstrated a definitive interaction between the virus and disease until now.

More than 130,000 new cases of NPC are diagnosed worldwide annually, with the majority of cases occurring in Southeast Asia, China, and Northern Africa. Men are three times more commonly affected than women.

In Singapore, the incidence of NPC is among the highest globally, with around 300 new cases diagnosed each year. Detection typically occurs late due to mild or nonspecific early symptoms, resulting in delayed diagnosis, poorer prognosis, and reduced treatment success rates.

The findings from the NTU-Chiba University team could lead to new treatments for NPC by targeting the genes affected by EBV. This would involve developing treatments that specifically interfere with the activity of these genes, such as drugs or therapies that block the function of the genes that EBV activates, thereby preventing tumour growth or even killing cancer cells.

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