{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,5]],"date-time":"2026-06-05T17:13:05Z","timestamp":1780679585333,"version":"3.54.1"},"reference-count":60,"publisher":"SAGE Publications","issue":"12","license":[{"start":{"date-parts":[[2014,4,1]],"date-time":"2014-04-01T00:00:00Z","timestamp":1396310400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2014,4,1]],"date-time":"2014-04-01T00:00:00Z","timestamp":1396310400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Antioxidants &amp; Redox Signaling"],"published-print":{"date-parts":[[2014,4]]},"abstract":"<jats:p>\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Aims:<\/jats:italic>\n                    <\/jats:bold>\n                    We have recently shown that fenretinide preferentially targets CD34\n                    <jats:sup>+<\/jats:sup>\n                    cells of acute myeloid leukemia (AML), and here, we test whether this agent exerts the effect on CD34\n                    <jats:sup>+<\/jats:sup>\n                    cells of chronic myeloid leukemia (CML), which are refractory to imatinib.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Results:<\/jats:italic>\n                    <\/jats:bold>\n                    As tested by colony-forming cell assays using clinical specimens, both number and size of total colonies derived from CD34\n                    <jats:sup>+<\/jats:sup>\n                    CML cells were significantly reduced by fenretinide, and by combining fenretinide with imatinib. In particular, colonies derived from erythroid progenitors and more primitive pluripotent\/multipotent progenitors were highly sensitive to fenretinide\/fenretinide plus imatinib. Accordantly, fenretinide appeared to induce apoptosis in CD34\n                    <jats:sup>+<\/jats:sup>\n                    CML cells, particularly with regard to the cells in the subpopulation of CD34\n                    <jats:sup>+<\/jats:sup>\n                    CD38\n                    <jats:sup>\u2212<\/jats:sup>\n                    . Through cell quiescent assays, including Ki-67 negativity test, we added evidence that nonproliferative CD34\n                    <jats:sup>+<\/jats:sup>\n                    CML cells were largely eliminated by fenretinide. Transcriptome and molecular data further showed that mechanisms underlying the apoptosis in CD34\n                    <jats:sup>+<\/jats:sup>\n                    CML cells were highly complex, involving multiple events of oxidative stress responses.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Innovation and Conclusion:<\/jats:italic>\n                    <\/jats:bold>\n                    As compared with CD34\n                    <jats:sup>+<\/jats:sup>\n                    AML cells, the apoptotic effects of fenretinide on CD34\n                    <jats:sup>+<\/jats:sup>\n                    CML cells were more prominent whereas less varied among the samples of different patients, and also various stress-responsive events appeared to be more robust in fenretinide-treated CD34\n                    <jats:sup>+<\/jats:sup>\n                    CML cells. Thus, the combination of fenretinide with imatinib may represent a more sophisticated strategy for CML treatment, in which imatinib mainly targets leukemic blast cells through the intrinsic pathway of apopotosis, whereas fenretinide primarily targets CML stem\/progenitor cells through the oxidative\/endoplasmic reticulum stress-mediated pathway.\n                    <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                    20, 1866\u20131880.\n                  <\/jats:p>","DOI":"10.1089\/ars.2012.4935","type":"journal-article","created":{"date-parts":[[2013,9,11]],"date-time":"2013-09-11T08:03:08Z","timestamp":1378886588000},"page":"1866-1880","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":16,"title":["Fenretinide Targets Chronic Myeloid Leukemia Stem\/Progenitor Cells by Regulation of Redox Signaling"],"prefix":"10.1177","volume":"20","author":[{"given":"Yanzhi","family":"Du","sequence":"first","affiliation":[{"name":"Shanghai Jiao Tong University School of Medicine (SJTU-SM)","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuan","family":"Xia","sequence":"additional","affiliation":[{"name":"Shanghai Jiao Tong University School of Medicine (SJTU-SM)","place":["China"]},{"name":"Graduate School of the Chinese Academy of Sciences","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoling","family":"Pan","sequence":"additional","affiliation":[{"name":"Shanghai Jiao Tong University School of Medicine (SJTU-SM)","place":["China"]},{"name":"Graduate School of the Chinese Academy of Sciences","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zi","family":"Chen","sequence":"additional","affiliation":[{"name":"Huashan Hospital Affiliated to Fudan University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aihua","family":"Wang","sequence":"additional","affiliation":[{"name":"Ruijin Hospital","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kankan","family":"Wang","sequence":"additional","affiliation":[{"name":"Ruijin Hospital","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junmin","family":"Li","sequence":"additional","affiliation":[{"name":"Ruijin Hospital","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ji","family":"Zhang","sequence":"additional","affiliation":[{"name":"Shanghai Jiao Tong University School of Medicine (SJTU-SM)","place":["China"]},{"name":"Ruijin Hospital","place":["China"]},{"name":"Ruijin Hospital","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2014,4,20]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkm883"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1357-2725(97)00135-0"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2002-09-2780"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)80595-4"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2005-07-2947"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjc.6603672"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI35721"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2004-04-1335"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-03-1484"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa062867"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1038\/nm0596-561"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2005-06-2318"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.devcel.2010.06.014"},{"key":"e_1_3_3_15_2","first-page":"2032","article-title":"Phase I trial and pharmacokinetics of fenretinide in children with neuroblastoma","volume":"9","author":"Garaventa A","year":"2003","unstructured":"Garaventa A, , Luksch R, , Lo Piccolo MS, , Cavadini E, , Montaldo PG, , Pizzitola MR, , Boni L, , Ponzoni M, , Decensi A, , De Bernardi B, , Bellani FF, , and Formelli F. 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