Schistosoma mansoni infection: Is it a risk factor for development of hepatocellular carcinoma?

El-Tonsy, Manar Mahmoud; Helal, Thanaa; Tawfik, Rania Ayman; Koriem, Khaled M. M.; Hussein, H. S.

doi:10.1016/j.actatropica.2013.07.024

Cited by 38 publications

(32 citation statements)

References 24 publications

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“…Among the parasitic agents proven to be carcinogenic for humans are Schistosoma haematobium and Schistosoma japonicum , associated with the occurrence of bladder cancer and hepatocellular carcinoma [42, 43], and Opisthorchis viverrini and Clonorchis sinensis associated with cholangiocarcinoma [44, 45]. In contrast to these data, there is a growing body of evidence that parasitic infections or application of parasite-derived proteins can suppress tumour growth.…”

Section: Discussionmentioning

confidence: 99%

Experimental immunology Necrosis and apoptosis in Trichinella spiralis -mediated tumour reduction

Vasilev¹,

Ilić²,

Gruden-Movsesijan³

et al. 2015

cejoi

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It is known that infection with different pathogens, including helminths, can alter the progression of malignant or other diseases. We studied the effect of chronic Trichinella spiralis infection or muscle larvae excretory-secretory (ES L1) antigens on the malignant tumour growth in the mouse melanoma model system in vivo and in vitro. Our results confirmed that chronic infection with T. spiralis possesses the capacity to slow down the progression of tumour growth, resulting in an impressive reduction in tumour size. We found that the phenomenon could, at least partially, be related to a lower level of tumour necrosis compared to necrosis present in control animals with progressive malignancy course. An increased apoptotic potential among the low percentage of cells within the total tumour cell number in vivo was also observed. ES L1 antigen, as a parasitic product that is released during the chronic phase of infection, reduced the survival and slightly, but significantly increased the apoptosis level of melanoma cells in vitro. Our results imply that powerful Trichinella anti-malignance capacity does not rely only on necrosis and apoptosis but other mechanisms through which infection or parasite products manipulate the tumor establishment and expansion should be considered.

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Section: Discussionmentioning

confidence: 99%

Experimental immunology Necrosis and apoptosis in Trichinella spiralis -mediated tumour reduction

Vasilev¹,

Ilić²,

Gruden-Movsesijan³

et al. 2015

cejoi

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“…(10) Clinical studies and animal experiments have suggested that schistosomiasis promotes the development of HCC but also colorectal cancer, prostate cancer, and giant follicular lymphomas. (11,12) Furthermore, schistosomiasis likely potentiates hepatic injury when coinciding with hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. (10) S. mansoni infection in a mouse model for HCC accelerated hepatic dysplastic changes and promoted earlier onset of cancer formation with a more aggressive nature.…”

Section: See Editorial On Page 375mentioning

confidence: 99%

“…(8) c-Jun and STAT3 are proto-oncogenes or transcription factors whose activation promotes the development and progression of dysplasia during HCC tumorigenesis. (11,14) In 2001, a clinical study initially suggested that the coordinated expression of c-fos and c-jun in HCC may reflect the coordinated tumor cell cycle of progression and proliferation. (16) c-Jun is a major regulator of hepatocyte survival (17) and hepatocyte proliferation during regeneration.…”

Section: Article Informationmentioning

confidence: 99%

Schistosoma mansoni Egg–Secreted Antigens Activate Hepatocellular Carcinoma–Associated Transcription Factors c‐Jun and STAT3 in Hamster and Human Hepatocytes

et al. 2019

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Clinical data have provided evidence that schistosomiasis can promote hepatocellular carcinogenesis. c-Jun and STAT3 are critical regulators of liver cancer development and progression. The aim of the present study was to investigate the hepatocellular activation of c-Jun and STAT3 by Schistosoma mansoni-infection. Expression and function of c-Jun, STAT3 as well as proliferation and DNA repair were analyzed by Western blotting, electrophoretic mobility shift assay, and immunohistochemistry in liver of S. mansoni-infected hamsters, Huh7 cells, primary hepatocytes, and human liver biopsies. Hepatocellular activation of c-Jun was demonstrated by nuclear translocation of c-Jun, enhanced phosphorylation (Ser73), and AP-1/DNA-binding in response to S. mansoni infection. Nuclear c-Jun staining pattern around lodged eggs without ambient immune reaction, and directionally from granuloma to the central veins suggested that substances released from schistosome eggs were responsible for the observed effects. In addition, hepatocytes with c-Jun activation, show cell activation and DNA double-strand breaks. These findings from the hamster model were confirmed by analyses of human biopsies from patients with schistosomiasis. Cell culture experiments finally demonstrated that activation of c-Jun and STAT3 as well as DNA repair were induced by an extract from schistosome eggs (soluble egg antigens (SEA) and culture supernatants of live schistosome egg (egg-conditioned medium (ECM)), and in particular by IPSE/alpha-1, the major component secreted by live schistosome eggs. The permanent activation of hepatocellular carcinoma-associated proto-oncogenes such as c-Jun and associated transcription factors including STAT3 by substances released from tissue-trapped schistosome eggs may be important factors contributing to the development of liver cancer in S. mansoni-infected patients. Therefore, identification and therapeutic targeting of the underlying pathways is a useful strategy to prevent schistosomiasis associated carcinogenesis. This article is protected by copyright. All rights reserved.

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“…Abgesehen von den chronischen Hepatitis-B-und/oder -C- [ weiteren Infektionskrankheiten bekannt, die mit einem erhöhten Risiko für ein HCC einhergehen. Es wurde in einer Reihe von Fallberichten über die Koexistenz eines HCC mit verschiedenen Infektionskrankheiten berichtetdarunter die Schistosomiasis [26,27], das SEN-Virus [28,29], das GB-C-Virus C [30] und das TT-Virus [31]. Auch ein Zusammenhang mit Helicobacter pylori wurde postuliert [32].…”

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Zystische Echinokokkose und hepatozelluläres Karzinom – zufällige Koinzidenz? Ein Fallbericht

et al. 2014

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The coincidence of HCC and cystic echinococcosis in the non-cirrhotic liver of a young man is a rare event. Despite resection in healthy tissue multicentric HCC was diagnosed 5 months later. Only few cases of simultaneous occurrence of HCC and echinococcosis have been published so far. Some authors considered echinococcosis as a trigger for HCC. A causal link between both entities has not been demonstrated until now.

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Schistosoma mansoni infection: Is it a risk factor for development of hepatocellular carcinoma?

Cited by 38 publications

References 24 publications

Experimental immunology Necrosis and apoptosis in Trichinella spiralis -mediated tumour reduction

Experimental immunology Necrosis and apoptosis in Trichinella spiralis -mediated tumour reduction

Schistosoma mansoni Egg–Secreted Antigens Activate Hepatocellular Carcinoma–Associated Transcription Factors c‐Jun and STAT3 in Hamster and Human Hepatocytes

Zystische Echinokokkose und hepatozelluläres Karzinom – zufällige Koinzidenz? Ein Fallbericht

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