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Liver fluke induces cholangiocarcinoma.

Sripa B, Kaewkes S, Sithithaworn P, Mairiang E, Laha T, Smout M, Pairojkul C, Bhudhisawasdi V, Tesana S, Thinkamrop B, Bethony JM, Loukas A, Brindley PJ - PLoS Med. (2007)

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Khon Kaen University, Khon Kaen, Thailand. banchob@kku.ac.th

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Proposed Mechanisms of Opisthorchis-Derived CCA InitiationThe three proposed pathways linking the parasite to CCA initiation are mechanical damage (in yellow), molecular products (in blue), and immunopathology (in green). Combined, these mechanisms result in several common elements (purple) that all lead to DNA damage. The inhibition of a normal DNA damage response is the final oncogenic factor proposed to dramatically increase the likelihood of a malignant transformation. This invariably leads to progression of CCA. (Adapted from [10].) The photographs underneath the schematic show two livers with advanced CCA.
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pmed-0040201.g005: Proposed Mechanisms of Opisthorchis-Derived CCA InitiationThe three proposed pathways linking the parasite to CCA initiation are mechanical damage (in yellow), molecular products (in blue), and immunopathology (in green). Combined, these mechanisms result in several common elements (purple) that all lead to DNA damage. The inhibition of a normal DNA damage response is the final oncogenic factor proposed to dramatically increase the likelihood of a malignant transformation. This invariably leads to progression of CCA. (Adapted from [10].) The photographs underneath the schematic show two livers with advanced CCA.

Mentions: Multi-factorial aetiology of CCA. Liver fluke–induced CCA is therefore generally accepted to be the result of chronic inflammation [53,58,59]. Several mechanisms by which O. viverrini infection may enhance cholangiocarcinogenesis have been proposed above, and are summarised in Figure 5. Indeed, it is almost certain that a combination of those pathologies described above (mechanical damage, parasite secretions, and immunopathology) culminate in CCA after chronic infection with O. viverrini. The primary pathologic change, i.e., epithelial desquamation, may be due to mechanical irritation caused by the liver fluke and/or its metabolic products. However, immunopathologic processes may contribute to the long-standing hepatobiliary damage. During liver fluke infection, inflammation, periductal fibrosis, and proliferative responses, including epithelial hyperplasia, goblet cell metaplasia, and adenomatous hyperplasia, may represent predisposing lesions that enhance susceptibility of DNA to carcinogens [11,60]. Several N-nitroso compounds and their precursors occur at low levels in fermented food such as preserved mud fish paste, pla-ra, a condiment that is a ubiquitous component of the cuisine of northeastern Thailand and Laos.


Liver fluke induces cholangiocarcinoma.

Sripa B, Kaewkes S, Sithithaworn P, Mairiang E, Laha T, Smout M, Pairojkul C, Bhudhisawasdi V, Tesana S, Thinkamrop B, Bethony JM, Loukas A, Brindley PJ - PLoS Med. (2007)

Proposed Mechanisms of Opisthorchis-Derived CCA InitiationThe three proposed pathways linking the parasite to CCA initiation are mechanical damage (in yellow), molecular products (in blue), and immunopathology (in green). Combined, these mechanisms result in several common elements (purple) that all lead to DNA damage. The inhibition of a normal DNA damage response is the final oncogenic factor proposed to dramatically increase the likelihood of a malignant transformation. This invariably leads to progression of CCA. (Adapted from [10].) The photographs underneath the schematic show two livers with advanced CCA.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC1913093&req=5

pmed-0040201.g005: Proposed Mechanisms of Opisthorchis-Derived CCA InitiationThe three proposed pathways linking the parasite to CCA initiation are mechanical damage (in yellow), molecular products (in blue), and immunopathology (in green). Combined, these mechanisms result in several common elements (purple) that all lead to DNA damage. The inhibition of a normal DNA damage response is the final oncogenic factor proposed to dramatically increase the likelihood of a malignant transformation. This invariably leads to progression of CCA. (Adapted from [10].) The photographs underneath the schematic show two livers with advanced CCA.
Mentions: Multi-factorial aetiology of CCA. Liver fluke–induced CCA is therefore generally accepted to be the result of chronic inflammation [53,58,59]. Several mechanisms by which O. viverrini infection may enhance cholangiocarcinogenesis have been proposed above, and are summarised in Figure 5. Indeed, it is almost certain that a combination of those pathologies described above (mechanical damage, parasite secretions, and immunopathology) culminate in CCA after chronic infection with O. viverrini. The primary pathologic change, i.e., epithelial desquamation, may be due to mechanical irritation caused by the liver fluke and/or its metabolic products. However, immunopathologic processes may contribute to the long-standing hepatobiliary damage. During liver fluke infection, inflammation, periductal fibrosis, and proliferative responses, including epithelial hyperplasia, goblet cell metaplasia, and adenomatous hyperplasia, may represent predisposing lesions that enhance susceptibility of DNA to carcinogens [11,60]. Several N-nitroso compounds and their precursors occur at low levels in fermented food such as preserved mud fish paste, pla-ra, a condiment that is a ubiquitous component of the cuisine of northeastern Thailand and Laos.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Khon Kaen University, Khon Kaen, Thailand. banchob@kku.ac.th

Show MeSH
Related in: MedlinePlus