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However, the molecular mechanism involved in chronic myeloid leukaemia (<jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content>), especially imatinib\u2010resistant <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> cells, is not completely understood. In the present study, we investigated the effect of <jats:styled-content style=\"fixed-case\">EGCG<\/jats:styled-content> on the growth of Bcr\/Abl+ <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> cell lines, including imatinib\u2010resistant cell lines and primary <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> cells. The results revealed that <jats:styled-content style=\"fixed-case\">EGCG<\/jats:styled-content> could inhibit cell growth and induce apoptosis in <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> cells. The mechanisms involved inhibition of the Bcr\/Abl oncoprotein and regulation of its downstream p38\u2010<jats:styled-content style=\"fixed-case\">MAPK<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">JNK<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>2\/<jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>3\/<jats:styled-content style=\"fixed-case\">AKT<\/jats:styled-content> pathways. In conclusion, we documented the anti\u2010<jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> effects of <jats:styled-content style=\"fixed-case\">EGCG<\/jats:styled-content> in imatinib\u2010sensitive and imatinib\u2010resistant Bcr\/Abl+ cells, especially T315I\u2010mutated cells.<\/jats:p>","DOI":"10.1111\/1440-1681.13037","type":"journal-article","created":{"date-parts":[[2018,9,25]],"date-time":"2018-09-25T08:53:40Z","timestamp":1537865620000},"page":"126-136","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":44,"title":["(\u2212)\u2010Epigallocatechin\u20103\u2010gallate induces cell apoptosis in chronic myeloid leukaemia by regulating Bcr\/Abl\u2010mediated p38\u2010<scp>MAPK<\/scp>\/<scp>JNK<\/scp> and <scp>JAK<\/scp>2\/<scp>STAT<\/scp>3\/<scp>AKT<\/scp> signalling pathways"],"prefix":"10.1111","volume":"46","author":[{"given":"Xiang","family":"Xiao","sequence":"first","affiliation":[{"name":"Department 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