A recent study published in the Journal of Medical Virology reveals that FDA-approved PARP1 inhibitors, such as talazoparib, can effectively combat EBV-driven lymphomas by disrupting the interaction between the viral protein EBNA2 and the oncogene MYC, which are critical for cancer progression.

Unlike their typical role in preventing DNA damage repair, these PARP inhibitors in EBV-positive cancers do not increase DNA damage but instead block the activity of the PARP1 enzyme, halting tumor growth.

In mouse models, treatment with talazoparib resulted in an 80% reduction in tumor growth and decreased cancer spread, demonstrating significant therapeutic potential without the DNA damage usually associated with these drugs.

Researchers at The Wistar Institute have identified that these FDA-approved PARP inhibitors can stop the growth of EBV-driven lymphomas, opening a promising new treatment pathway for these aggressive cancers.

Given the established safety profile of PARP inhibitors like talazoparib, their repurposing for EBV-related cancers could be expedited, and ongoing research is exploring their effects on other EBV-driven malignancies such as nasopharyngeal and gastric cancers.

Since over 90% of the global population is infected with EBV, and immunocompromised individuals are at higher risk of developing EBV-associated cancers, these findings could fill a significant gap where current therapies do not target EBV-specific pathways.

Translating basic virology insights into targeted therapies offers new hope for patients with limited options, emphasizing the importance of this research in advancing treatment for EBV-related cancers.

Beyond oncology, the research team is investigating PARP1’s role in autoimmune diseases linked to EBV, indicating broader implications for understanding how EBV impacts gene regulation and disease.

The study highlights that the inhibition of PARP1 disrupts the interaction between EBV's EBNA2 protein and the MYC oncogene, which is essential for cancer development, rather than causing DNA damage.

The research also involved testing the PARP inhibitor on mice, which showed a significant decrease in tumor growth and spread, demonstrating the potential for clinical application.

Researchers are also exploring the effectiveness of PARP inhibitors against other EBV-related cancers, such as nasopharyngeal and gastric carcinomas, broadening the scope of this promising therapeutic approach.

This discovery suggests that existing PARP1 inhibitors could be repurposed to target EBV's ability to hijack cellular machinery, offering a new strategy beyond their traditional use in DNA repair.