Analysis of adenomatous polyposis coli gene expression, APC locus-microsatellite instability and APC promoter methylation in the progression of melanocytic tumours

Korabiowska, M; Schlott, Thilo; Siems, Nils; Müller, Anegret; Cordon‐Cardo, Carlos; Fischer, Gösta; Brinck, Ulrich

doi:10.1038/modpathol.3800238

Cited by 16 publications

(15 citation statements)

References 25 publications

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“…Interestingly, high levels of ␤-catenin have been observed in malignant melanomas. Furthermore, activating mutations in the ␤-catenin gene (CTNNB1), as well as genetic and epigenetic alterations of the APC gene, occur in malignant melanomas and are associated with melanoma progression (26,48,62). Thus, as in colon cancer, aberrant Wnt signaling is relevant to the genesis and progression of melanomas.…”

Section: Resultsmentioning

confidence: 99%

E-Cadherin Is Required for Caveolin-1-Mediated Down-Regulation of the Inhibitor of Apoptosis Protein Survivin via Reduced β-Catenin-Tcf/Lef-Dependent Transcription

Torres

Tapia

Rodríguez

et al. 2007

Molecular and Cellular Biology

102

120

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Caveolin-1 reportedly acts as a tumor suppressor and promotes events associated with tumor progression, including metastasis. The molecular mechanisms underlying such radical differences in function are not understood. Recently, we showed that caveolin-1 inhibits expression of the inhibitor of apoptosis protein survivin via a transcriptional mechanism involving the ␤-catenin-Tcf/Lef pathway. Surprisingly, while caveolin-1 expression decreased survivin mRNA and protein levels in HT29 (

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Section: Resultsmentioning

confidence: 99%

E-Cadherin Is Required for Caveolin-1-Mediated Down-Regulation of the Inhibitor of Apoptosis Protein Survivin via Reduced β-Catenin-Tcf/Lef-Dependent Transcription

Torres

Tapia

Rodríguez

et al. 2007

Molecular and Cellular Biology

102

120

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“…BRAF mutations, often observed in cutaneous melanoma, were not found in uveal melanomas 12 13. Hypermethylation of RASSF1, RARB and APC has been identified in cutaneous melanoma 14 – 16. However, except for RASSF1 in one recent study,10 these epigenetic events have not been investigated in uveal melanoma.…”

mentioning

confidence: 94%

Methylation of CpG island promoters in uveal melanoma

Moulin

Clément

Bosman

et al. 2008

British Journal of Ophthalmology

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Background: Inactivation of tumour-related genes by promoter hypermethylation is a common epigenetic event in the development of a variety of tumours. Aim: To investigate in primary uveal melanoma the status of promoter methylation of genes thought to be involved in tumour development: p16, TIMP3, RASSF1, RARB, FHIT, hTERT and APC. Methods: Gene promoter methylation was studied by methylation-sensitive single-strand conformation analysis and dot-blot assay in a series of 23 primary uveal melanomas. All DNA samples were obtained from paraffin-embedded formalin-fixed tissue blocks. Results: hTERT promoter methylation was found with a relatively high frequency (52%). Promoter methylation of p16, TIMP3, RASSF1, RARB, FHIT and APC was a rare event. For none of these genes did promoter methylation exceed 15% of tumour samples, and, for some genes (FHIT and APC), no methylation was found at all. Furthermore, promoter methylation was absent in 39% (9/ 23) of cases. In only 22% (5/23) of cases was hypermethylation of at least two promoters observed. Conclusions: Promoter methylation of hTERT is a regular event in uveal melanoma. Hypermethylation of the other genes studied does not seem to be an essential element in the development of this tumour. As promoter methylation of APC, RASSF1 and RARB is often observed in cutaneous melanoma, these results suggest that different epigenetic events occur in the development of cutaneous and uveal melanoma.Uveal melanoma is the most common primary intraocular tumour in adults, with a stable incidence of 4.3 new cases per million per year over the last 25 years.1 Despite new treatment modalities, mortality has not decreased, 2 mainly because of liver metastases. Although numerous studies have addressed the genetic events involved in the development of uveal melanoma, only a few have focused on the epigenetic events that may occur during tumorigenesis.CpG islands promoter methylation, associated with transcriptional gene silencing, has emerged as one of the most important epigenetic alterations in the development of human malignancies.3 Promoter methylation has been observed in many tumour types, 4 5 but there are few reports on uveal melanoma. p16 promoter has been found to be methylated in up to 32% of primary tumours and 50% of cell lines. [6][7][8] In derived cell lines, TIMP3 expression was found to be lower in liver metastatic cells than primary uveal tumour, and it was suggested that TIMP3 promoter methylation may be the cause of TIMP3 downregulation. 9 More recently, RASSF1 promoter methylation was identified in 50% of primary uveal melanoma, and a correlation was noticed between RASSF1 promoter methylation status and the development of metastasis. 10Although cutaneous and uveal melanoma share common morphological features, they differ substantially in their behaviour, metastatic spread and response to chemotherapy. There is increasing evidence that this is related to differences in their molecular phenotype. cDNA analysis has revealed that uveal and cutaneous melanoma...

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“…non-human primates. Rats treated with CCl 4 were used to serve as an in vivo halogenated hydrocarbon-induced liver injury model (Korabiowska et al, 2004). In the present study, CCl 4 stimulated oxidative stress, as indicated by the elevated level of TBARS and the decreased level of SOD activity in the liver of the rats, which would further induce lipid peroxidation, initial free radical damage to the hepatocyte membrane and eventually lead to the liver injury (Andus et al, 1991).…”

Section: Discussionmentioning

confidence: 96%

“…CCl 4 has been shown to induce oxidative stress, leading to lipid peroxidation and free radical production, which plays an important pathological role in liver injury (Korabiowska et al, 2004). The effect of rBPTI on lipid peroxidation products, measured as TBARS in the liver, is shown in Figure 4(a).…”

Section: Rbpti Reduces Oxidative Stress In Ratsmentioning

confidence: 99%

Recombinant bovine pancreatic trypsin inhibitor protects the liver from carbon tetrachloride-induced chronic injury in rats

Dong¹,

Lv²,

Wang

et al. 2013

Pharmaceutical Biology

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(2013) Recombinant bovine pancreatic trypsin inhibitor protects the liver from carbon tetrachloride-induced chronic injury in rats, Pharmaceutical Biology, 51:10, 1298-1303, DOI: 10.3109/13880209.2013 Context: Bovine pancreatic trypsin inhibitor (BPTI) has been reported to relieve liver ischemiareperfusion-induced injury in rats. Objective: This study was designed to determine whether the recombinant BPTI (rBPTI) can prevent the chronic liver injury induced by CCl 4 in rats. Materials and methods: Fifty male Wistar rats were divided into five groups. Rats were treated with 40% CCl 4 at a dose of 2 ml/kg body weight twice a week subcutaneously for 12 weeks. In the 8th week, they were administered intraperitoneally with rBPTI (80 MU/kg), BPTI (80 MU/kg) or hepatocyte growth-promoting factor (pHGF; 100 mg/kg) daily for the next 4 weeks. Results: rBPTI significantly prevented the disruption of liver function of alanine aminotransferase (ALT; 172.7 AE 18.16 versus 141.2 AE 15.28, p ¼ 0.003), aspartate aminotransferase (AST; 225.10 AE 36.54 versus 170.06 AE 27.14, p ¼ 0.007) and hydroxyproline (Hyp; 1.14 AE 0.27 versus 0.62 AE 0.17, p ¼ 0.001). rBPTI significantly decreased the level of thiobarbituric acid reactive substances (TBARS; 1.15 AE 0.16 versus 0.87 AE 0.15, p ¼ 0.003) and increased the activities of superoxide dismutase (SOD; 6.07 AE 0.95 versus 7.75 AE 1.12, p ¼ 0.007). rBPTI reduced the production of cytokines of IL-1b and TGF-b. The hepatocyte necrosis, fibrosis, fatty degeneration and inflammatory cell infiltration were ameliorated by rBPTI administration. Conclusion: This study demonstrated that rBPTI exerted a hepatoprotective effect on chronic liver fibrosis induced by CCl 4 , which suggests that rBPTI may have the potential application for chronic liver injury induced by drugs metabolism and toxic substances.

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Analysis of adenomatous polyposis coli gene expression, APC locus-microsatellite instability and APC promoter methylation in the progression of melanocytic tumours

Cited by 16 publications

References 25 publications

E-Cadherin Is Required for Caveolin-1-Mediated Down-Regulation of the Inhibitor of Apoptosis Protein Survivin via Reduced β-Catenin-Tcf/Lef-Dependent Transcription

E-Cadherin Is Required for Caveolin-1-Mediated Down-Regulation of the Inhibitor of Apoptosis Protein Survivin via Reduced β-Catenin-Tcf/Lef-Dependent Transcription

Methylation of CpG island promoters in uveal melanoma

Recombinant bovine pancreatic trypsin inhibitor protects the liver from carbon tetrachloride-induced chronic injury in rats

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