A Lymphotoxin-Driven Pathway to Hepatocellular Carcinoma

Haybaeck, Johannes; Zeller, Nicolas; Wolf, Monika; Weber, Achim; Wagner, Ulrich; Kurrer, Michael; Bremer, Juliane; Iezzi, Giovanna; Graf, Rolf; Clavien, Pierre‐Alain; Thimme, Robert; Blum, Hubert E.; Nedospasov, Sergei A.; Zatloukal, Kurt; Ramzan, Muhammad; Ciesek, Sandra; Pietschmann, Thomas; Marche, Patrice N.; Karin, Michael; Köpf, Manfred; Browning, Jeffrey L.; Aguzzi, Adriano; Heikenwälder, Mathias

doi:10.1016/j.ccr.2009.10.004

Cited by 105 publications

(219 citation statements)

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“…In most of these diseases, elevated expression of LT or its target genes has been detected, supporting LT's role in lymphoid neogenesis (Drayton et al, 2006). Suppression of LTbR signaling by injection of LTbR-Ig was efficacious in the treatment of various inflammatory or autoimmune disease models (Gommerman and Browning, 2003;Ware, 2005;Drayton et al, 2006;Browning, 2008;Haybaeck et al, 2009). …”

Section: Lt and Inflammationmentioning

confidence: 93%

“…Interestingly, LTbR activation (through LIGHT or LTab heterotrimers) can also activate the canonical NF-kB (Dejardin et al, 2002;Muller and Siebenlist, 2003;Haybaeck et al, 2009).…”

Section: Ltbr Activation and Nf-jb Signalingmentioning

confidence: 99%

“…The role of LT in the context of lymphoid neogenesis, development of autoimmune diseases and inflammatory disorders was further investigated in vivo (Picarella et al, 1992;Kratz et al, 1996;Luther et al, 2000;Drayton et al, 2003Drayton et al, , 2006Gommerman and Browning, 2003;Martin et al, 2004;Heikenwalder et al, 2005Heikenwalder et al, , 2008Haybaeck et al, 2009). These studies revealed that ectopic LT expression suffices to generate lymphoid-like structures (Picarella et al, 1992;Kratz et al, 1996;Gommerman and Browning, 2003;Heikenwalder et al, 2005;Haybaeck et al, 2009), also termed tertiary lymphoid organs or tissues.…”

Section: Lt and Inflammationmentioning

confidence: 99%

“…These studies revealed that ectopic LT expression suffices to generate lymphoid-like structures (Picarella et al, 1992;Kratz et al, 1996;Gommerman and Browning, 2003;Heikenwalder et al, 2005;Haybaeck et al, 2009), also termed tertiary lymphoid organs or tissues. LTa or LTab expression under the control of the rat insulin promoter II (RIP) induces chemokine expression and follicular lymphocytic infiltrations with mature follicular dendritic cell networks, resulting in chronic insulitis and glomerulonephritis (Picarella et al, 1992;Kratz et al, 1996;Drayton et al, 2003).…”

Section: Lt and Inflammationmentioning

confidence: 99%

“…Patients suffering from HBV-or HCV-induced chronic hepatitis or HCC displayed increased hepatic expression of LTa, LTb and LTbR (Haybaeck et al, 2009). But which cell type is responsible for the elevated expression of LT in chronic HCV-infected patients?…”

Section: Hepatic Ltbr Signaling and Hccmentioning

confidence: 99%

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The unexpected role of lymphotoxin β receptor signaling in carcinogenesis: from lymphoid tissue formation to liver and prostate cancer development

et al. 2010

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Section: Lt and Inflammationmentioning

confidence: 93%

“…Interestingly, LTbR activation (through LIGHT or LTab heterotrimers) can also activate the canonical NF-kB (Dejardin et al, 2002;Muller and Siebenlist, 2003;Haybaeck et al, 2009).…”

Section: Ltbr Activation and Nf-jb Signalingmentioning

confidence: 99%

Section: Lt and Inflammationmentioning

confidence: 99%

Section: Lt and Inflammationmentioning

confidence: 99%

Section: Hepatic Ltbr Signaling and Hccmentioning

confidence: 99%

See 3 more Smart Citations

The unexpected role of lymphotoxin β receptor signaling in carcinogenesis: from lymphoid tissue formation to liver and prostate cancer development

et al. 2010

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Modeling Human Liver Cancer Heterogeneity: Virally Induced Transgenic Models and Mouse Genetic Models of Chronic Liver Inflammation

Ringelhan

Reisinger²,

Yuan³

et al. 2014

CP Pharmacology

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In addition to being the most common primary liver cancer, hepatocellular carcinoma (HCC) is the second most common cause of cancer-related death in humans. Treatment options are limited for this chemoresistant cancer, with liver transplantation and surgical intervention in early stages being the most successful treatments. Drug development over the past 15 years has focused on generating mouse models that mimic the human pathology for HCC. This has enabled the laboratory testing of potentially new human therapeutics. Described in this unit are the classification of HCC and an overview of hepatitis virus-related transgenic and genetically engineered mouse models (GEMMs) that are employed for elucidating the mechanism(s) responsible for the development of HCC, with particular emphasis on genetic, dietary, and environmental factors.

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