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Parasitic Infections and Carcinogenesis: Molecular Mechanisms, Immune Modulation, and Emerging Therapeutic Strategies
Marta Pawłowska1, Dorian Jarek2, Jan Milanowski2
1Department of Medical Biology and Biochemistry, Faculty of Medicine, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, 24 Karłowicza St., Bydgoszcz, 85-092, Poland.
Abstract:
Parasitic infections are increasingly recognized as contributors to cancer development, yet the underlying oncogenic mechanisms remain insufficiently understood. Growing evidence from molecular oncology, immunology, and microbiome research suggests that chronic parasitic infections may drive tumorigenesis through sustained inflammation, deregulated signaling pathways, genomic instability, and the release of parasite-derived exosomes that reshape the tumor microenvironment. These insights underscore the need to integrate parasitology with cancer biology to understand infection-associated malignancies better. The aim of this narrative review is to synthesize current knowledge on how selected parasites contribute to cancer development and to highlight emerging therapeutic and diagnostic opportunities. We examine pathogens such as Schistosoma haematobium, Opisthorchis viverrini, Toxoplasma gondii, Plasmodium falciparum, and Leishmania spp., detailing their roles in chronic inflammation, immune modulation, and interactions with tumor-associated immune cells. The review further discusses parasite-induced immunosuppression, coinfections, and their cumulative impact on cancer risk. Additionally, we explore novel therapeutic approaches, including pathway inhibitors, epigenetic drugs, microbiome modulation, and engineered parasites. Future perspectives emphasize parasite-based immunotherapies, long-term epigenetic consequences of infection, and AI-driven multi-omics strategies for identifying oncogenic signatures. This review integrates advances from parasitology and oncology to provide new insights into biomarkers, targeted therapies, and mechanisms of infection-induced tumorigenesis. The literature search covered studies indexed in PubMed, Scopus, and Web of Science up to July 2025.
Insights
Chronic parasitic infections contribute to cancer by causing inflammation and altering the tumor environment. This review explores mechanisms and new therapies for infection-associated cancers.
Area of Science:
- Integrates parasitology, molecular oncology, immunology, and microbiome research.
- Focuses on infection-associated malignancies and tumorigenesis.
Background:
- Parasitic infections are increasingly linked to cancer development.
- Oncogenic mechanisms are not fully understood, but involve chronic inflammation, immune modulation, and parasite exosomes.
- Selected parasites include *Schistosoma haematobium*, *Opisthorchis viverrini*, *Toxoplasma gondii*, *Plasmodium falciparum*, and *Leishmania* spp.
Purpose of the Study:
- To synthesize current knowledge on how parasites contribute to cancer development.
- To highlight emerging therapeutic and diagnostic opportunities.
- To integrate parasitology and cancer biology for understanding infection-associated malignancies.
Main Methods:
- Narrative review of literature indexed in PubMed, Scopus, and Web of Science up to July 2025.
- Examination of parasite roles in chronic inflammation, immune modulation, and tumor microenvironment.
- Exploration of parasite-induced immunosuppression, coinfections, and their impact on cancer risk.
Main Results:
- Parasites drive tumorigenesis via sustained inflammation, deregulated pathways, genomic instability, and exosomes.
- Parasites modulate immune responses and interact with tumor-associated immune cells.
- Novel therapeutic approaches include pathway inhibitors, epigenetic drugs, microbiome modulation, and engineered parasites.
Conclusions:
- Understanding parasite-cancer links requires integrating parasitology and oncology.
- Future research should focus on parasite-based immunotherapies, epigenetic effects, and AI-driven multi-omics.
- Advances offer new insights into biomarkers, targeted therapies, and infection-induced tumorigenesis mechanisms.
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