title: Activated DDR1 increases RS cell survival.
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.
authors.affiliation: CENTRO DI RIFERIMENTO ONCOLOGICO;
authors.forename: Antonino
authors.initials: A
authors.lastname: Carbone
authors.forename: Annunziata
authors.initials: A
authors.lastname: Gloghini
mesh_terms: D001402:B-Lymphocytes / Q000166:cytology*; D000070819:Discoidin Domain Receptor 1; D020031:Epstein-Barr Virus Infections / Q000235:genetics*; D004854:Herpesvirus 4, Human / Q000235:genetics*; D006689:Hodgkin Disease / Q000235:genetics*; D006801:Humans; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism*; D014763:Viral Matrix Proteins / Q000235:genetics*
chemical_list: C037662:EBV-associated membrane antigen, Epstein-Barr virus; D014763:Viral Matrix Proteins; C092030:DDR1 protein, human; D000070819:Discoidin Domain Receptor 1; D020794:Receptor Protein-Tyrosine Kinases