2008
DOI: 10.1016/j.yexmp.2007.12.003
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Fat10 is an epigenetic marker for liver preneoplasia in a drug-primed mouse model of tumorigenesis

Abstract: There is clinical evidence that chronic liver diseases in which MDBs (Mallory Denk Bodies) form progress to hepatocellular carcinoma. The present study provides evidence that links MDB formation induced by chronic drug injury, with preneoplasia and later to the formation of tumors, which develop long after drug withdrawal. Evidence indicated that this link was due to an epigenetic cellular memory induced by chronic drug ingestion. Microarray analysis showed that the expressions of many markers of preneoplasia … Show more

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Cited by 57 publications
(93 citation statements)
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“…In fact, in NIH3T3 colony formation assays FAT10 failed to exert transforming activity (Figure 4). Our data do not rule out that other factors such as transcriptional reprogramming, the formation of Mallory-Denk bodies (Oliva et al, 2008) or the loss of p53 may contribute to FAT10 overexpression to a minor extent but the striking coexpression of FAT10 and LMP2 can not be explained if these other factors would be major determinants of FAT10 expression.…”
Section: Fat10 Upregulation By Proinflammatory Cytokinescontrasting
confidence: 75%
See 1 more Smart Citation
“…In fact, in NIH3T3 colony formation assays FAT10 failed to exert transforming activity (Figure 4). Our data do not rule out that other factors such as transcriptional reprogramming, the formation of Mallory-Denk bodies (Oliva et al, 2008) or the loss of p53 may contribute to FAT10 overexpression to a minor extent but the striking coexpression of FAT10 and LMP2 can not be explained if these other factors would be major determinants of FAT10 expression.…”
Section: Fat10 Upregulation By Proinflammatory Cytokinescontrasting
confidence: 75%
“…The argument that no FAT10 expression was found in healthy liver tissue from the same patient is not necessarily in conflict with this possibility as the liver is a large organ and an immune response may be confined to the vicinity of the tumor lesion. The notion that nonmalignant cells in the surrounding of HCC lesions also upregulated FAT10 expression was very recently confirmed in a study on chemically induced HCC in mice where FAT10-positive hepatocytes were found located close to the tumor and blood vessels (Oliva et al, 2008). However, no evidence for chromosomal aberrations was found in FAT10-positive HCC T and C HCC 50…”
Section: Fat10 Upregulation By Proinflammatory Cytokinesmentioning
confidence: 90%
“…In addition to Topo IIα, upregulation of Ubd has been shown in preneoplastic lesions and carcinomas in mouse hepatocarcinogenesis models (Oliva et al, 2008;French et al, 2011). However, in the present study, the number of Ubd + cells did not increase within preneoplastic lesions in the liver and thyroid.…”
Section: Discussioncontrasting
confidence: 84%
“…In liver neoplasia FAT10 is even described as an epigenetic marker (French et al, 2010a,b;Oliva et al, 2008). Moreover, in several cancer types a statistically significant association between a high FAT10 expression level and the progression and severity of the disease including a higher propensity for metastasis formation and poor prognosis, has been reported.…”
Section: Fat10 Expression Levels In Different Cancer Typesmentioning
confidence: 99%