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DNA damage forms the basic mechanism of cancer cell eradication in current therapy of AML.<\/jats:p>\n            <jats:p>Hdm2 and pro-apoptotic Bcl-2 members are among the most intensely induced genes immediately after chemotherapy and Hdm2 is proposed a role in receptor tyrosine kinase regulation. Thus we examined the DNA damage related modulation of these proteins in relation to <jats:italic>FLT3<\/jats:italic> mutational status and induction of apoptosis.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>Within one hour after exposure to ionizing radiation (IR), the AML cells (NB4, MV4-11, HL-60, primary AML cells) showed an increase in Flt3 protein independent of mRNA levels, while the Hdm2 protein decreased. The <jats:italic>FLT3<\/jats:italic> mutant MV4-11 cells were resistant to IR accompanied by presence of both Mcl-1 and Hdm2 protein three hours after IR. In contrast, the <jats:italic>FLT3<\/jats:italic> wild type NB4 cells responded to IR with apoptosis and pre-apoptotic Mcl-1 down regulation. Daunorubicin (DNR) induced continuing down regulation of Hdm2 and Mcl-1 in both cell lines followed by apoptosis.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p>Both IR and DNR treatment resulted in concerted protein modulations of Mcl-1, Hdm2 and Flt3. Cell death induction was associated with persistent attenuation of Mcl-1 and Hdm2. These observations suggest that defining the pathway(s) modulating Flt3, Hdm2 and Mcl-1 may propose new strategies to optimize therapy for the relapse prone <jats:italic>FLT3<\/jats:italic> mutated AML patients.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1476-4598-6-33","type":"journal-article","created":{"date-parts":[[2007,5,12]],"date-time":"2007-05-12T06:13:35Z","timestamp":1178950415000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Pre-apoptotic response to therapeutic DNA damage involves protein modulation of Mcl-1, Hdm2 and Flt3 in acute myeloid leukemia cells"],"prefix":"10.1186","volume":"6","author":[{"given":"Line","family":"Wergeland","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gry","family":"Sj\u00f8holt","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ingvild","family":"Haaland","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Randi","family":"Hovland","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"\u00d8ystein","family":"Bruserud","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bj\u00f8rn Tore","family":"Gjertsen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2007,5,11]]},"reference":[{"issue":"3","key":"241_CR1","doi-asserted-by":"publisher","first-page":"197","DOI":"10.1016\/j.critrevonc.2003.11.002","volume":"50","author":"M Smith","year":"2004","unstructured":"Smith M, Barnett M, Bassan R, Gatta G, Tondini C, Kern W: Adult acute myeloid leukaemia. 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