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Epstein-Barr virus and the origin of Hodgkin lymphoma.

Vockerodt M, Cader FZ, Shannon-Lowe C, Murray P - Chin J Cancer (2014)

Bottom Line: Although Epstein-Barr virus (EBV) is present in the malignant Hodgkin/Reed-Sternberg (HRS) cells of a proportion of cases of classical Hodgkin lymphoma (cHL), how the virus contributes to the pathogenesis of this disease remains poorly defined.It is clear from the studies of other EBV-associated cancers that the virus is usually not sufficient for tumor development and that other oncogenic co-factors are required.This article reviews what is known about the contribution of EBV to the pathogenesis of cHL and focuses on emerging evidence implicating chronic inflammation as a potential oncogenic co-factor in this malignancy.

View Article: PubMed Central - PubMed

Affiliation: School of Cancer Sciences, University of Birmingham, Birmingham, B15 2TT, the United Kingdom. p.g.murray@bham.ac.uk.

ABSTRACT
Although Epstein-Barr virus (EBV) is present in the malignant Hodgkin/Reed-Sternberg (HRS) cells of a proportion of cases of classical Hodgkin lymphoma (cHL), how the virus contributes to the pathogenesis of this disease remains poorly defined. It is clear from the studies of other EBV-associated cancers that the virus is usually not sufficient for tumor development and that other oncogenic co-factors are required. This article reviews what is known about the contribution of EBV to the pathogenesis of cHL and focuses on emerging evidence implicating chronic inflammation as a potential oncogenic co-factor in this malignancy.

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Related in: MedlinePlus

Potential role for collagen in activating the oncogenic functions of LMP1.LMP1 can induce expression of the collagen receptor, discoidin domain receptor 1 (DDR1), in the normal EBV-infected GC B cell (indicated by red arrow). During a chronic inflammatory response, collagen is deposited in the microenvironment of the EBV-infected cell and can activate DDR1, leading to growth-promoting signaling.
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cjc-33-12-591-g002: Potential role for collagen in activating the oncogenic functions of LMP1.LMP1 can induce expression of the collagen receptor, discoidin domain receptor 1 (DDR1), in the normal EBV-infected GC B cell (indicated by red arrow). During a chronic inflammatory response, collagen is deposited in the microenvironment of the EBV-infected cell and can activate DDR1, leading to growth-promoting signaling.

Mentions: In addition to regulating EBV expression, there is emerging evidence that the microenvironment can also modulate the function of individual virus proteins. For example, we have shown that LMP1 can induce the expression of the collagen receptor, discoidin domain receptor 1 (DDR1). This is important because collagen is a major constituent of the chronic inflammatory microenvironment of cHL[79]–[82]. Ligation of DDR1 by collagen promotes the survival of lymphoma cells in vitro, suggesting that the excess collagen present in lymphomas could drive some oncogenic functions of LMP1[82] (Figure 2). Changes to the microenvironment of the infected B cell might help to explain why on the one hand LMP1 expression in the asymptomatic host provides only those signals required to drive the differentiation of EBV-infected GC B cells, yet on the other hand, LMP1 has potentially oncogenic functions. An important area of future research will be to unravel the complex interactions between the EBV-infected B cell and its microenvironment and to determine how disruption or modification of these interactions might be tumor-promoting.


Epstein-Barr virus and the origin of Hodgkin lymphoma.

Vockerodt M, Cader FZ, Shannon-Lowe C, Murray P - Chin J Cancer (2014)

Potential role for collagen in activating the oncogenic functions of LMP1.LMP1 can induce expression of the collagen receptor, discoidin domain receptor 1 (DDR1), in the normal EBV-infected GC B cell (indicated by red arrow). During a chronic inflammatory response, collagen is deposited in the microenvironment of the EBV-infected cell and can activate DDR1, leading to growth-promoting signaling.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4308654&req=5

cjc-33-12-591-g002: Potential role for collagen in activating the oncogenic functions of LMP1.LMP1 can induce expression of the collagen receptor, discoidin domain receptor 1 (DDR1), in the normal EBV-infected GC B cell (indicated by red arrow). During a chronic inflammatory response, collagen is deposited in the microenvironment of the EBV-infected cell and can activate DDR1, leading to growth-promoting signaling.
Mentions: In addition to regulating EBV expression, there is emerging evidence that the microenvironment can also modulate the function of individual virus proteins. For example, we have shown that LMP1 can induce the expression of the collagen receptor, discoidin domain receptor 1 (DDR1). This is important because collagen is a major constituent of the chronic inflammatory microenvironment of cHL[79]–[82]. Ligation of DDR1 by collagen promotes the survival of lymphoma cells in vitro, suggesting that the excess collagen present in lymphomas could drive some oncogenic functions of LMP1[82] (Figure 2). Changes to the microenvironment of the infected B cell might help to explain why on the one hand LMP1 expression in the asymptomatic host provides only those signals required to drive the differentiation of EBV-infected GC B cells, yet on the other hand, LMP1 has potentially oncogenic functions. An important area of future research will be to unravel the complex interactions between the EBV-infected B cell and its microenvironment and to determine how disruption or modification of these interactions might be tumor-promoting.

Bottom Line: Although Epstein-Barr virus (EBV) is present in the malignant Hodgkin/Reed-Sternberg (HRS) cells of a proportion of cases of classical Hodgkin lymphoma (cHL), how the virus contributes to the pathogenesis of this disease remains poorly defined.It is clear from the studies of other EBV-associated cancers that the virus is usually not sufficient for tumor development and that other oncogenic co-factors are required.This article reviews what is known about the contribution of EBV to the pathogenesis of cHL and focuses on emerging evidence implicating chronic inflammation as a potential oncogenic co-factor in this malignancy.

View Article: PubMed Central - PubMed

Affiliation: School of Cancer Sciences, University of Birmingham, Birmingham, B15 2TT, the United Kingdom. p.g.murray@bham.ac.uk.

ABSTRACT
Although Epstein-Barr virus (EBV) is present in the malignant Hodgkin/Reed-Sternberg (HRS) cells of a proportion of cases of classical Hodgkin lymphoma (cHL), how the virus contributes to the pathogenesis of this disease remains poorly defined. It is clear from the studies of other EBV-associated cancers that the virus is usually not sufficient for tumor development and that other oncogenic co-factors are required. This article reviews what is known about the contribution of EBV to the pathogenesis of cHL and focuses on emerging evidence implicating chronic inflammation as a potential oncogenic co-factor in this malignancy.

Show MeSH
Related in: MedlinePlus