{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T16:18:34Z","timestamp":1776269914373,"version":"3.50.1"},"reference-count":69,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2011,2,8]],"date-time":"2011-02-08T00:00:00Z","timestamp":1297123200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes Chromosomes &amp;amp; Cancer"],"published-print":{"date-parts":[[2011,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Recent developments in genomic technologies have resulted in increased understanding of pathogenic mechanisms and emphasized the importance of central survival pathways. Here, we use a novel bioinformatic based integrative genomic profiling approach to elucidate conserved mechanisms of lymphomagenesis in the three commonest non\u2010Hodgkin's lymphoma (NHL) entities: diffuse large B\u2010cell lymphoma, follicular lymphoma, and B\u2010cell chronic lymphocytic leukemia. By integrating genome\u2010wide DNA copy number analysis and transcriptome profiling of tumor cohorts, we identified genetic lesions present in each entity and highlighted their likely target genes. This revealed a significant enrichment of components of both the apoptosis pathway and the mitogen activated protein kinase pathway, including amplification of the <jats:italic>MAP3K12<\/jats:italic> locus in all three entities, within the set of genes targeted by genetic alterations in these diseases. Furthermore, amplification of 12p13.33 was identified in all three entities and found to target the <jats:italic>FOXM1<\/jats:italic> oncogene. Amplification of <jats:italic>FOXM1<\/jats:italic> was subsequently found to be associated with an increased MYC oncogenic signaling signature, and siRNA\u2010mediated knock\u2010down of <jats:italic>FOXM1<\/jats:italic> resulted in decreased MYC expression and induced G2 arrest. Together, these findings underscore genetic alteration of the MAPK and apoptosis pathways, and genetic amplification of <jats:italic>FOXM1<\/jats:italic> as conserved mechanisms of lymphomagenesis in common NHL entities. Integrative genomic profiling identifies common central survival mechanisms and highlights them as attractive targets for directed therapy. \u00a9 2011 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/gcc.20856","type":"journal-article","created":{"date-parts":[[2011,2,9]],"date-time":"2011-02-09T11:56:39Z","timestamp":1297252599000},"page":"313-326","source":"Crossref","is-referenced-by-count":43,"title":["Integrative genomic profiling reveals conserved genetic mechanisms for tumorigenesis in common entities of non\u2010Hodgkin's lymphoma"],"prefix":"10.1002","volume":"50","author":[{"given":"Michael R.","family":"Green","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carlos","family":"Aya\u2010Bonilla","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maher 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