Researchers have made a groundbreaking discovery in the fight against ovarian cancer, identifying eTreg cells as a new immunotherapy target for high-grade serous ovarian cancer (HGSOC). This breakthrough could lead to innovative treatment strategies tailored to individual patients.

Ovarian cancer, particularly HGSOC, remains one of the top ten malignant tumors in women, with HGSOC accounting for nearly 70 percent of these cases. For many patients, especially those with tumors too difficult to remove surgically, the standard treatment involves platinum-based neoadjuvant chemotherapy. While this approach often achieves high response rates initially, it frequently leads to drug resistance over time. Consequently, the five-year survival rate for these patients has stagnated around 30 percent, highlighting a critical need for better treatments.

A key factor in the development of HGSOC is homologous recombination deficiency (HRD), a condition where cells struggle to repair DNA double-strand breaks through the homologous recombination pathway. This deficiency not only increases the risk of cancer development but also affects treatment strategies.

A collaborative study between Tongji Hospital in China and MD Anderson Cancer Center in the United States explored the potential of neoadjuvant PARP inhibitor niraparib for HRD-positive HGSOC, using a reverse translational medicine approach. PARP inhibitors block enzymes involved in DNA repair, preventing cancer cells, especially those with HRD, from fixing DNA damage, thereby promoting cell death.

Over four years, the researchers delved into the immune characteristics of the HGSOC microenvironment, employing single-cell transcriptome sequencing and T-cell receptor sequencing to screen thousands of potential targets. Gao Qinglei, a professor at Tongji Hospital, explained that they identified a novel immune target: eTreg cells in HRD-positive ovarian cancer. They proposed a new immunotherapy strategy that focuses on depleting eTreg cells while activating immune cells to effectively combat the tumors.

Furthermore, they developed HRD mouse models and discovered that depleting eTregs, with or without PARP inhibition, significantly suppressed tumor growth without causing observable toxicities. This suggests that targeting eTregs could be a promising therapeutic approach for HGSOC and other HRD-related tumors.

This significant study has been published in the prestigious journal Cell, offering new hope for more effective treatments for ovarian cancer.

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