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CML blasts have constitutive p65 (RelA NF-\u03baB) transcriptional activity, and NF-\u03baB may be a potential target for molecular therapies in CML that may also be effective against CML cells with Bcr-Abl-T315I.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>In this report, we discovered that pristimerin, a quinonemethide triterpenoid isolated from Celastraceae and Hippocrateaceae, inhibited growth and induced apoptosis in CML cells, including the cells harboring Bcr-Abl-T315I mutation. Additionally, pristimerin inhibited the growth of imatinib-resistant Bcr-Abl-T315I xenografts in nude mice. Pristimerin blocked the TNF\u03b1-induced I\u03baB\u03b1 phosphorylation, translocation of p65, and expression of NF-\u03baB-regulated genes. Pristimerin inhibited two steps in NF-\u03baB signaling: TAK1\u2192IKK and IKK\u2192I\u03baB\u03b1. Pristimerin potently inhibited two pairs of CML cell lines (KBM5 versus KBM5-T315I, 32D-Bcr-Abl versus 32D-Bcr-Abl-T315I) and primary cells from a CML patient with acquired resistance to imatinib. The mRNA and protein levels of Bcr-Abl in imatinib-sensitive (KBM5) or imatinib-resistant (KBM5-T315I) CML cells were reduced after pristimerin treatment. Further, inactivation of Bcr-Abl by imatinib pretreatment did not abrogate the TNF\u03b1-induced NF-\u03baB activation while silencing p65 by siRNA did not affect the levels of Bcr-Abl, both results together indicating that NF-\u03baB inactivation and Bcr-Abl inhibition may be parallel independent pathways.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>To our knowledge, this is the first report to show that pristimerin is effective <jats:italic>in vitro<\/jats:italic> and <jats:italic>in vivo<\/jats:italic> against CML cells, including those with the T315I mutation. The mechanisms may involve inhibition of NF-\u03baB and Bcr-Abl. We concluded that pristimerin could be a lead compound for further drug development to overcome imatinib resistance in CML patients.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/1476-4598-9-112","type":"journal-article","created":{"date-parts":[[2010,5,19]],"date-time":"2010-05-19T18:14:43Z","timestamp":1274292883000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":62,"title":["Pristimerin induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation by blocking NF-\u03baB signaling and depleting Bcr-Abl"],"prefix":"10.1186","volume":"9","author":[{"given":"Zhongzheng","family":"Lu","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yanli","family":"Jin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chun","family":"Chen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Juan","family":"Li","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qi","family":"Cao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jingxuan","family":"Pan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2010,5,19]]},"reference":[{"key":"627_CR1","doi-asserted-by":"publisher","first-page":"441","DOI":"10.1038\/nrc2147","volume":"7","author":"JV Melo","year":"2007","unstructured":"Melo JV, Barnes DJ: Chronic myeloid leukaemia as a model of disease evolution in human cancer. 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