Abstract
In this issue of Blood, Cader et al show that tumor microenvironment promotes Epstein-Barr virus (EBV)-driven lymphomagenesis in Hodgkin lymphoma by a novel pathway involving latent membrane protein 1 (LMP1) and discoidin domain receptor 1 (DDR1), which is activated by collagen(s) and contributes to the survival of Reed-Sternberg (RS) cells.
MeSH terms
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B-Lymphocytes / cytology*
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Discoidin Domain Receptor 1
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Epstein-Barr Virus Infections / genetics*
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Herpesvirus 4, Human / genetics*
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Hodgkin Disease / genetics*
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Humans
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Receptor Protein-Tyrosine Kinases / metabolism*
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Viral Matrix Proteins / genetics*
Substances
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EBV-associated membrane antigen, Epstein-Barr virus
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Viral Matrix Proteins
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DDR1 protein, human
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Discoidin Domain Receptor 1
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Receptor Protein-Tyrosine Kinases