{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T03:59:33Z","timestamp":1791518373048,"version":"4.3.4"},"reference-count":130,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2013,7,26]],"date-time":"2013-07-26T00:00:00Z","timestamp":1374796800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2013,8]]},"abstract":"Chronic myeloid leukaemia (CML<\/jats:styled-content>) is a clonal myeloproliferative disorder characterized by the presence of a fusion oncogene BCR\u2010ABL<\/jats:styled-content>, which encodes a protein with constitutive TK activity. The implementation of tyrosine kinase inhibitors (TKIs<\/jats:styled-content>) marked a major advance in CML<\/jats:styled-content> therapy; however, there are problems with current treatment. For example, relapse occurs when these drugs are discontinued in the majority of patients who have achieved a complete molecular response on TKI<\/jats:styled-content> and these agents are less effective in patients with mutations in the BCR\u2010ABL<\/jats:styled-content> kinase domain. Importantly, TKI<\/jats:styled-content> can effectively target proliferating mature cells, but do not eradicate quiescent leukaemic stem cells (LSCs<\/jats:styled-content>), therefore allowing disease persistence despite treatment. It is essential that alternative strategies are used to target the LSC<\/jats:styled-content> population. BCR\u2010ABL<\/jats:styled-content> activation is responsible for the modulation of different signalling pathways, which allows the LSC<\/jats:styled-content> fraction to evade cell death. Several pathways have been shown to be modulated by BCR\u2010ABL<\/jats:styled-content>, including PI3K\/AKT\/mTOR<\/jats:styled-content>, JAK\u2010STAT<\/jats:styled-content> and autophagy signalling pathways. Targeting components of these survival pathways, alone or in combination with TKI<\/jats:styled-content>, therefore represents an attractive potential therapeutic approach for targeting the LSC<\/jats:styled-content>. However, many pathways are also active in normal stem cells. Therefore, potential targets must be validated to effectively eradicate CML<\/jats:styled-content> stem cells while sparing normal counterparts. This review summarizes the main pathways modulated in CML<\/jats:styled-content> stem cells, the recent developments and the use of novel drugs to target components in these pathways which may be used to target the LSC<\/jats:styled-content> population.<\/jats:p><\/jats:sec>Linked Articles<\/jats:title>This article is part of a themed section on Emerging Therapeutic Aspects in Oncology. 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