A newly presented study has uncovered troubling molecular changes in the cervix associated with a common parasitic infection, Schistosoma haematobium, and its standard treatment.
The research, shared at the ESCMID Global 2025 conference on April 12, indicates that this parasitic disease, already known to cause bladder cancer, may also influence cervical cancer risk by altering gene expression in infected women, particularly after treatment.
Schistosoma haematobium, responsible for urogenital schistosomiasis, affects more than 110 million people worldwide, primarily in areas with limited access to clean water and sanitation.
While its role in bladder cancer is well-established, its potential to impact the cervix at the genetic level has remained largely unexplored until now. Researchers studied cervical tissue from 39 women in Tanzania, comparing those infected with S. haematobium (n=20) to those uninfected (n=19).
After administering the antiparasitic drug praziquantel to infected participants, they tracked changes in gene activity over a period of 4 to 12 months using RNA sequencing.
The results were striking: nine genes showed significant differences between infected and uninfected women, 23 genes shifted in those who cleared the infection after treatment, and 29 genes differed between post-treatment and never-infected individuals.
Several of these genes are directly involved in cancer-related processes. Among the genes most affected were: BLK proto-oncogene, which regulates cell growth and may drive tumor development when overactive; Long Intergenic Non-Protein Coding RNA 2084, a marker associated with poor cancer prognosis; Trichohyalin, linked to abnormal keratin formation in certain cancers; TCL1 AKT coactivator A, a known promoter of cell survival involved in blood cancers.
Even more concerning, post-treatment samples revealed enhanced activity in biological pathways associated with inflammation, angiogenesis, and tissue breakdown, processes that can compromise the cervix’s structural defenses and increase susceptibility to human papillomavirus (HPV), the leading cause of cervical cancer.
“The findings suggest that infection may trigger molecular changes that make women more vulnerable to cancer-related processes in the cervix, especially after treatment,” said Dr Anna Maria Mertelsmann, the study’s lead author.
She noted the unexpected downregulation of claudins and tight junction proteins, which help maintain the cervical lining’s integrity. Their reduction could, she warned, pave the way for HPV to infect and persist in cervical cells.
“Women who received praziquantel treatment exhibited more genetic changes linked to cancer than those with an active infection,” Dr Mertelsmann added.
“This raises critical questions about the long-term effects of treatment and highlights the need for careful post-treatment monitoring,” Dr Mertelsmann said.
A larger follow-up study tracking 180 women over a full year is now underway to validate these results. The team also plans to explore how schistosomiasis may interact with long-term HPV infection to influence cervical cancer risk.
Dr Mertelsmann called for increased global awareness of Female Genital Schistosomiasis (FGS), a frequently underdiagnosed condition, and emphasized the need for early screening in women previously infected with S. haematobium. She also proposed that adjunct treatments, such as immune-modulating or anti-inflammatory therapies, might help counteract the gene-level changes observed post-treatment.
In parallel, she underlined the critical role of widespread HPV vaccination as a preventive measure for populations at risk.
(With inputs from ANI)
