A groundbreaking study presented at ESCMID Global 2025 has unveiled a concerning link between Schistosoma haematobium, a parasitic infection affecting over 110 million individuals globally, and the activation of cancer-related genes in cervical tissue. The research highlights how this often-neglected disease may increase the risk of cervical cancer through molecular changes that persist even after treatment with praziquantel. By analyzing cervical samples from Tanzanian women, researchers identified significant genetic alterations associated with oncogenic pathways, raising critical questions about long-term health impacts.

The study focused on S. haematobium, a major cause of schistosomiasis, which primarily affects regions lacking clean water and sanitation. While its association with bladder cancer is well-documented, its potential role in cervical malignancies has been less explored. Researchers examined cervical tissues from infected and uninfected women, both before and after treatment. Using advanced RNA sequencing techniques, they discovered nine genes expressed differently between infected and uninfected groups. Four of these were directly linked to cancer mechanisms, including BLK proto-oncogene, which influences cell proliferation, and trichohyalin, involved in keratin complex formation.

Post-treatment analyses revealed an unexpected rise in activity within certain cancer-related biological pathways. These included processes tied to inflammation, tissue remodeling, and compromised protective barriers in the cervix. Such changes could lead to increased blood vessel formation, tumor-promoting activities, and reduced apoptosis—a natural process for eliminating abnormal cells. Lead author Dr. Anna Maria Mertelsmann noted that treated women exhibited more pronounced genetic changes compared to those with active infections, emphasizing the importance of post-treatment monitoring.

Beyond immediate effects, the study suggests that S. haematobium might weaken cervical tissue integrity by downregulating key protective genes like claudins and tight junction proteins. This vulnerability could exacerbate HPV infections, a leading cause of cervical cancer. Ongoing research involving 180 participants aims to validate these findings over a longer period, while future investigations will assess whether prolonged HPV persistence heightens cancer risks among women previously infected with schistosomiasis.

Dr. Mertelsmann advocates for heightened awareness of Female Genital Schistosomiasis (FGS), urging closer surveillance of infected women for early signs of cervical abnormalities. She also proposes supplementary therapies such as anti-inflammatory or immune-modulating treatments to mitigate adverse effects following praziquantel administration. Furthermore, widespread HPV vaccination campaigns could significantly reduce cervical cancer incidence among affected populations, offering hope for improved public health outcomes.