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Review
. 2017 Jul 27;13(7):e1006393.
doi: 10.1371/journal.ppat.1006393. eCollection 2017 Jul.

Helminth infection-induced malignancy

Paul J Brindley  1   2 , Alex Loukas  3
Affiliations
Review

Helminth infection-induced malignancy

Paul J Brindley et al. PLoS Pathog. .
No abstract available

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Schematic representation of hypothesized processes of carcinogenesis of the biliary tract and urinary bladder during chronic infection with fish-borne liver flukes Opisthorchis viverrini (Ov) and Clonorchis sinensis (Cs) and the blood fluke Schistosoma haematobium (Sh).
Photomicrographs: adult developmental stages of Cs and Ov and the egg stage of Sh. During infection, mutations initiate carcinogenesis, perhaps as the consequence of interaction of epithelial cell chromosomal DNA with inflammation-associated reactive oxygen species (ROS) and reactive nitrogen species (RNS) and lipid peroxidation and/or metabolites released by the worms, such as catechol estrogen quinones and oxysterols. Subsequently, mediators of helminth origin such as granulin from Ov promote epidermal to mesenchymal transition (EMT), transformed cell growth, complementary angiogenesis, down-regulation of apoptosis, and other hallmarks of cancer.
Fig 2
Fig 2. Liver fluke granulin promotes wound repair and angiogenesis.
Opisthorchis viverrini secretes a growth factor termed liver fluke granulin, Ov-GRN-1, an orthologue of mammalian granulin. Ov-GRN-1 stimulates cholangiocytes to proliferate and promotes wound healing and angiogenesis. A recent report on Ov-GRN-1 [32] illustrates some of these carcinogenic-conducive properties of the growth factor, as follows: (A) rate of wound closure on a cutaneous lesion on mice, (B) the angiogenic nature of Ov-GRN-1 revealed using the chorioallantoic membrane assay in fertilized quail eggs.
See this image and copyright information in PMC

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