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To gain insights into the biological features underlying this presentation, we investigated the gene expression profile (GEP) and the <jats:italic>IGHV<\/jats:italic> mutational status in a cohort of leukaemic MCL cases. Comparison of MCL with other lymphoproliferative disorders (i.e. splenic marginal zone lymphoma, follicular lymphoma, chronic lymphocytic leukaemia) revealed a MCL signature enriched for the following gene categories: mitochondrion, oxidoreductase activity, response to stress, to DNA damage and <jats:italic>TP53<\/jats:italic>\u2010pathway. Furthermore, GEP analysis revealed that non\u2010nodal MCL cases were characterized by the down\u2010modulation of the following gene categories: cell projection, actin cytoskeleton organization, cell adhesion (<jats:italic>ITGAE<\/jats:italic>, <jats:italic>CELSR1, PCDH9<\/jats:italic>) and tumour invasion\/progression (<jats:italic>PGF<\/jats:italic>, <jats:italic>ST14<\/jats:italic>, <jats:italic>ETS1<\/jats:italic>, <jats:italic>OCIAD1, EZR<\/jats:italic>). Many down\u2010modulated genes were related to the <jats:italic>TP53<\/jats:italic>\u2010pathway and to DNA damage response. <jats:italic>IGHV<\/jats:italic> status proved unmutated in all nodal and mutated in all non\u2010nodal MCL. Non\u2010nodal leukaemic MCLs display a peculiar clinical presentation, with distinctive biological features, such as mutated <jats:italic>IGHV<\/jats:italic> and a transcriptional profile lacking tumour invasion properties, that might contribute to the absence of nodal involvement and to the less aggressive clinical course.<\/jats:p>","DOI":"10.1111\/j.1365-2141.2011.08962.x","type":"journal-article","created":{"date-parts":[[2011,12,8]],"date-time":"2011-12-08T10:43:26Z","timestamp":1323341006000},"page":"601-611","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Behind the scenes of non\u2010nodal MCL: downmodulation of genes involved in actin cytoskeleton organization, cell projection, cell adhesion, tumour invasion, <i>TP53<\/i> pathway and mutated status of immunoglobulin heavy chain genes"],"prefix":"10.1111","volume":"156","author":[{"given":"Ilaria","family":"Del 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