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Chromosomal abnormalities in<jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content>are predictive of the natural disease course; del(11q) and del(17p) are recognized as high risk genetic lesions. Del(17p) is associated with an impaired function of<jats:styled-content style=\"fixed-case\">TP<\/jats:styled-content>53, a key tumour suppressor, and is particularly problematic. Such patients respond poorly to chemo\u2010immunotherapy and have significantly shorter survival compared to patients with standard and low\u2010risk cytogenetics. While<jats:styled-content style=\"fixed-case\">TP<\/jats:styled-content>53 pathway defects are rare at initial diagnosis, their frequency increases in relapsed<jats:styled-content style=\"fixed-case\">CLL<\/jats:styled-content>. Until very recently, this group of patients represented an unmet clinical need with few therapeutic options. However, the advent of targeted therapies has expanded the drug armamentarium and introduced new hope for these highly refractory patients. Agents that target B\u2010cell receptor signalling,<jats:styled-content style=\"fixed-case\">BH<\/jats:styled-content>3\u2010mimetics and others induce apoptosis of the neoplastic B\u2010cells in a<jats:styled-content style=\"fixed-case\">TP<\/jats:styled-content>53\u2010independent manner. Their use in the clinic is associated with remarkable activity in patients with del(17p). In this review we discuss the frequency and clinical significance of del(17p) and genetic mutations leading to disrupted<jats:styled-content style=\"fixed-case\">TP<\/jats:styled-content>53, the putative role of other<jats:styled-content style=\"fixed-case\">TP<\/jats:styled-content>53 homologues, and the results of key clinical trials involving both conventional chemotherapy and novel agents.<\/jats:p>","DOI":"10.1111\/bjh.13042","type":"journal-article","created":{"date-parts":[[2014,7,21]],"date-time":"2014-07-21T05:17:48Z","timestamp":1405919868000},"page":"149-161","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["A new hope: novel therapeutic approaches to treatment of chronic lymphocytic leukaemia with defects in<i><scp>TP<\/scp>53<\/i>"],"prefix":"10.1111","volume":"167","author":[{"given":"Polina","family":"Shindiapina","sequence":"first","affiliation":[{"name":"Medicine Dartmouth\u2010Hitchcock Medical Center Lebanon NH USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jennifer R.","family":"Brown","sequence":"additional","affiliation":[{"name":"Medical Oncology Dana\u2010Farber Cancer Institute Boston MA USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alexey V.","family":"Danilov","sequence":"additional","affiliation":[{"name":"Medicine Dartmouth\u2010Hitchcock Medical Center Lebanon NH USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2014,7,21]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2011-03-341032"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1200\/JCO.2012.42.8623"},{"key":"e_1_2_7_4_1","volume-title":"2013 ASCO Annual Meeting, Vol. 31","author":"Barrientos J.C.","year":"2013"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1200\/JCO.2009.22.0442"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1080\/10428190701724801"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2007-12-129379"},{"key":"e_1_2_7_8_1","article-title":"Final results of a phase I study of idelalisib (GS\u20101101) a selective inhibitor of PI3K\u03b4, in patients with relapsed or refractory CLL","volume":"31","author":"Brown J.R.","year":"2013","journal-title":"Journal of Clinical Oncology (ASCO Annual Meeting Abstracts)"},{"key":"e_1_2_7_9_1","doi-asserted-by":"crossref","unstructured":"Brown J.R. 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