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Query: UMLS:C0851341 (infestation)
 10,121 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cholangiocarcinomas (CCs) are highly lethal malignant tumours arising from the biliary tract epithelium. The disease is notoriously difficult to diagnose and is usually fatal because of its typically late clinical presentation and the lack of effective non-surgical therapeutic modalities. The overall survival rate, including resected patients is poor, with less than 5% of patients surviving 5 years, a rate which has not changed significantly over the past 30 years. Although CC is a relatively uncommon tumor, interest in this disease is rising as incidence and mortality rates for intrahepatic cholangiocarcinoma are increasing markedly worldwide. A variety of risk factors, including primary sclerosing cholangitis, liver fluke infestation, and hepatolithiasis have been described. However, for most CCs the cause is unknown, and affected individuals have no history of exposure to, or association with, known risk factors. Recent advances in molecular pathogenesis have highlighted the importance of epigenetic alterations in the form of promoter region hypermethylation and histone deacetylation in addition to genetic changes in the process of cholangiocarcinogenesis. This review provides a comprehensive overview of the genes reported to be methylated in CC to date and their putative roles in cholangiocarcinogenesis. Future directions in the study of methylated genes and their potential roles as diagnostic and prognostic markers are also discussed.
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PMID:Epigenetic DNA hypermethylation in cholangiocarcinoma: potential roles in pathogenesis, diagnosis and identification of treatment targets. 1803 77

Cholangiocarcinoma (CCA) is a highly lethal malignant tumor arising from the biliary tract epithelium, characterized by its typically late clinical presentation and lack of effective therapeutic modalities. Chronic inflammatory conditions, including primary sclerosing cholangitis, liver fluke infestation and hepatolithiasis, are listed in the risk factors, but for most cases of CCA the cause is unknown. Recent advances in molecular pathogenesis have highlighted the importance of epigenetic alterations including promoter hypermethylation and histone deacetylation in addition to genetic changes in the process of cholangiocarcinogenesis. This review provides a comprehensive overview of the genes hypermethylated in CCA to date and their putative roles in cholangiocarcinogenesis. Among genes hypermethylated, we found the CpG island hypermethylation in suppressor of cytokine signaling 3 (SOCS3) gene promoter in CCA. Interleukin-6 (IL-6)-mediated signal transducers and activators of transcription 3 (STAT3) activation are aberrantly sustained in CCA cells, resulting in resistance to apoptosis. SOCS3 controls the IL-6/STAT3 signaling pathway by a classic feedback loop. Indeed, SOCS3 epigenetic silencing is responsible for sustained IL-6/STAT3 signaling in CCA. These findings provide new perspectives for epigenetic therapy to restore SOCS3 in this cancer.
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PMID:Epigenetic alterations in cholangiocarcinoma-sustained IL-6/STAT3 signaling in cholangio- carcinoma due to SOCS3 epigenetic silencing. 1915 83

Cholangiocarcinoma (CCA) is a highly lethal malignant tumor arising from the biliary tract epithelium. Chronic inflammatory conditions, including primary sclerosing cholangitis, liver fluke infestation, and hepatolithiasis, are considered risk factors, but the cause is still unknown in most cases. Recent advances in molecular pathogenesis have highlighted the importance of epigenetic alterations, including promoter hypermethylation and histone deacetylation, in the process of cholangiocarcinogenesis. More recently, research interest has been focusing on microRNA (mir), a major subtype of non-coding RNA. Mir is highly conserved among species and regulates the expression of specific target genes by binding to the 3'-untranslated regions of messenger RNA. The number of studies on a possible link between mir and various cancers is growing. This review provides a comprehensive overview of the genes currently known to be hypermethylated in CCA and their putative roles in cholangiocarcinogenesis. The epigenetic role of mir in the pathogenesis of CCA is also discussed.
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PMID:Epigenetic alterations associated with cholangiocarcinoma (review). 1957 60

Cholangiocarcinoma (CCA) is a notoriously lethal malignancy arising from the biliary tract epithelium. While relatively rare, incidence rates have increased markedly worldwide in the past decade. Although definite risk factors such as primary sclerosing cholangitis, liver fluke infestation, and hepatolithiasis have been well- documented, the cause of CCA remains unknown for most cases. An importance of not only genetic alterations but also epigenetic aberrations, including promoter hypermethylation and histone modifications, has been indicated for the processes of carcinogenesis and pathogenesis of CCA. This review focuses on epigenetic mechanisms involved in CCA genesis, with special emphasis on their applicability as potential biomarkers for diagnosis, prognosis and prediction as well as promising targets for novel therapeutic strategies.
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PMID:Epigenetic aberrations in cholangiocarcinoma: potential biomarkers and promising target for novel therapeutic strategies. 2348 Jul 63

Parasitoids are insects that use other insects as hosts. They sabotage host cellular and humoral defences to promote the survival of their offspring by injecting viruses and venoms along with their eggs. Many pathogens and parasites disrupt host epigenetic mechanisms to overcome immune system defences, and we hypothesized that parasitoids may use the same strategy. We used the ichneumon wasp Pimpla turionellae as a model idiobiont parasitoid to test this hypothesis, with pupae of the greater wax moth Galleria mellonella as the host. We found that parasitoid infestation involves the suppression of host immunity-related effector genes and the modulation of host genes involved in developmental hormone signalling. The transcriptional reprogramming of host genes following the injection of parasitoid eggs was associated with changes in host epigenetic mechanisms. The introduction of parasitoids resulted in a transient decrease in host global DNA methylation and the modulation of acetylation ratios for specific histones. Genes encoding regulators of histone acetylation and deacetylation were mostly downregulated in the parasitized pupae, suggesting that parasitoids can suppress host transcription. We also detected a strong parasitoid-specific effect on host microRNAs regulating gene expression at the post-transcriptional level. Our data therefore support the hypothesis that parasitoids may favour the survival of their offspring by interfering with host epigenetic mechanisms to suppress the immune system and disrupt development.
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PMID:Reprograming of epigenetic mechanisms controlling host insect immunity and development in response to egg-laying by a parasitoid wasp. 3251 98