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However, not all resistant patients harbour these alterations. We have performed a whole\u2010exome sequencing study to identify alternative molecular mechanisms that can drive ibrutinib resistance. Our findings include deletions on chromosomes 6q, including homozygous deletions, and 8p, which encompass key regulators of BTK, MYD88\/NF\u2010\u03baB, and apoptotic signalling. Moreover, we have identified recurring mutations in ubiquitin ligases, innate immune signalling, and TLR\/MYD88 pathway regulators in ibrutinib\u2010resistant WM patients.<\/jats:p>","DOI":"10.1111\/bjh.16463","type":"journal-article","created":{"date-parts":[[2020,2,27]],"date-time":"2020-02-27T08:21:06Z","timestamp":1582791666000},"page":"1165-1170","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["Genomic evolution of ibrutinib\u2010resistant clones in Waldenstr\u00f6m macroglobulinaemia"],"prefix":"10.1111","volume":"189","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5543-5154","authenticated-orcid":false,"given":"Cristina","family":"Jim\u00e9nez","sequence":"first","affiliation":[{"name":"Bing Center for Waldenstrom's Macroglobulinemia Dana\u2010Farber Cancer Institute Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gloria 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