Tumor-suppressor pathways in Schistosoma mansoni support a novel hypothesis on neodermatan flatworm origins

Authors

• Paul J. Brindley, Department of Microbiology, Immunology and Tropical Medicine, School of Medicine & Health Sciences, The George Washington University, Washington, DC 20037, USA. Electronic address: [email protected].

Document Type

Journal Article

Publication Date

4-1-2026

Journal

Trends in parasitology

Volume

42

Issue

4

DOI

10.1016/j.pt.2026.02.003

Keywords

cki; cyclin-dependent kinase inhibitor; horizontal gene transfer; parasitic flatworms; tegument

Abstract

Wendt and Collins identify a cyclin-dependent kinase inhibitor (cki) in Schistosoma mansoni that, along with p53-1 (schistosome homolog of TP-53), suppresses tegument cell proliferation. Knockdown of cki causes hyperproliferation and, together with p53-1 loss, tumorlike growths. Homologs of cki are widespread in parasitic flatworms but absent in free-living relatives, suggesting that the horizontal gene transfer aided the evolution of parasitism.

APA Citation

Brindley, Paul J., "Tumor-suppressor pathways in Schistosoma mansoni support a novel hypothesis on neodermatan flatworm origins" (2026). GW Authored Works. Paper 9162.
https://hsrc.himmelfarb.gwu.edu/gwhpubs/9162

Department

Microbiology, Immunology, and Tropical Medicine