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B\u2010cell lymphomas frequently (dys)regulate <jats:styled-content style=\"fixed-case\">BCR<\/jats:styled-content> signalling and thus take advantage of this pre\u2010existing pathway for B\u2010cell proliferation and survival. This has recently been underscored by clinical trials demonstrating that small molecules (fosfamatinib, ibrutinib, idelalisib) inhibiting <jats:styled-content style=\"fixed-case\">BCR<\/jats:styled-content>\u2010associated kinases (<jats:styled-content style=\"fixed-case\">SYK<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> BTK<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> PI<\/jats:styled-content>3K) have an encouraging clinical effect. Here we describe the current knowledge of the specific aspects of <jats:styled-content style=\"fixed-case\">BCR<\/jats:styled-content> signalling in diffuse large B\u2010cell lymphoma (<jats:styled-content style=\"fixed-case\">DLBCL<\/jats:styled-content>), follicular lymphoma, chronic lymphocytic leukaemia (<jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content>) and normal B cells. Multiple factors can contribute to <jats:styled-content style=\"fixed-case\">BCR<\/jats:styled-content> pathway (dys)regulation in these malignancies and the activation of \u2018chronic\u2019 or \u2018tonic\u2019 <jats:styled-content style=\"fixed-case\">BCR<\/jats:styled-content> signalling. In lymphoma B cells, the balance of initiation, amplitude and duration of <jats:styled-content style=\"fixed-case\">BCR<\/jats:styled-content> activation can be influenced by a specific immunoglobulin structure, the expression and mutations of adaptor molecules (like <jats:styled-content style=\"fixed-case\">GAB<\/jats:styled-content>1, <jats:styled-content style=\"fixed-case\">BLNK<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> GRB<\/jats:styled-content>2, <jats:styled-content style=\"fixed-case\">CARD<\/jats:styled-content>11), the activity of kinases (like <jats:styled-content style=\"fixed-case\">LYN<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> SYK<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> PI<\/jats:styled-content>3K) or phosphatases (like <jats:styled-content style=\"fixed-case\">SHIP<\/jats:styled-content>\u20101, <jats:styled-content style=\"fixed-case\">SHP<\/jats:styled-content>\u20101 and <jats:styled-content style=\"fixed-case\">PTEN<\/jats:styled-content>) and levels of micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s. We also discuss the crosstalk of <jats:styled-content style=\"fixed-case\">BCR<\/jats:styled-content> with other signalling pathways (<jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u03baB, adhesion through integrins, migration and chemokine signalling) to emphasise that the \u2018<jats:styled-content style=\"fixed-case\">BCR<\/jats:styled-content> inhibitors\u2019 target multiple pathways interconnected with <jats:styled-content style=\"fixed-case\">BCR<\/jats:styled-content>, which might explain some of their clinical activity.<\/jats:p>","DOI":"10.1111\/ejh.12427","type":"journal-article","created":{"date-parts":[[2014,8,1]],"date-time":"2014-08-01T07:48:18Z","timestamp":1406879298000},"page":"193-205","source":"Crossref","is-referenced-by-count":188,"title":["B\u2010cell receptor signalling and its crosstalk with other pathways in normal and malignant 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