{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T10:43:00Z","timestamp":1790678580224,"version":"4.1.0"},"reference-count":381,"publisher":"SAGE Publications","issue":"16","license":[{"start":{"date-parts":[[2015,6,1]],"date-time":"2015-06-01T00:00:00Z","timestamp":1433116800000},"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":[[2015,6]]},"abstract":"<jats:p>\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Significance:<\/jats:italic>\n                    <\/jats:bold>\n                    Chronic myeloid leukemia (CML) involves the malignant transformation of hematopoietic stem cells, defined largely by the Philadelphia chromosome and expression of the breakpoint cluster region-Abelson (BCR-ABL) oncoprotein. Pharmacological tyrosine kinase inhibitors (TKIs), including imatinib mesylate, have overcome limitations in conventional treatment for the improved clinical management of CML.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Recent Advances:<\/jats:italic>\n                    <\/jats:bold>\n                    Accumulated evidence has led to the identification of a subpopulation of quiescent leukemia progenitor cells with stem-like self renewal properties that may initiate leukemogenesis, which are also shown to be present in residual disease due to their insensitivity to tyrosine kinase inhibition.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Critical Issues:<\/jats:italic>\n                    <\/jats:bold>\n                    The characterization of quiescent leukemia progenitor cells as a unique cell population in CML pathogenesis has become critical with the complete elucidation of mechanisms involved in their survival independent of BCR-ABL that is important in the development of novel anticancer strategies. Understanding of these functional pathways in CML progenitor cells will allow for their selective therapeutic targeting. In addition, disease pathogenesis and drug responsiveness is also thought to be modulated by epigenetic regulatory mechanisms such as DNA methylation, histone acetylation, and microRNA expression, with a capacity to control CML-associated gene transcription.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Future Directions:<\/jats:italic>\n                    <\/jats:bold>\n                    A number of compounds in combination with TKIs are under preclinical and clinical investigation to assess their synergistic potential in targeting leukemic progenitor cells and\/or the epigenome in CML. Despite the collective promise, further research is required in order to refine understanding, and, ultimately, advance antileukemic therapeutic strategies.\n                    <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                    22, 1425\u20131462.\n                  <\/jats:p>","DOI":"10.1089\/ars.2014.6096","type":"journal-article","created":{"date-parts":[[2014,11,3]],"date-time":"2014-11-03T20:35:17Z","timestamp":1415046917000},"page":"1425-1462","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":10,"title":["The Implication of Cancer Progenitor Cells and the Role of Epigenetics in the Development of Novel Therapeutic Strategies for Chronic Myeloid Leukemia"],"prefix":"10.1177","volume":"22","author":[{"given":"Stephanie M.","family":"Tortorella","sequence":"first","affiliation":[{"name":"The Alfred Medical Research and Education Precinct","place":["Australia"]},{"name":"The University of Melbourne","place":["Australia"]},{"name":"The University of Melbourne","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew","family":"Hung","sequence":"additional","affiliation":[{"name":"RMIT University","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tom C.","family":"Karagiannis","sequence":"additional","affiliation":[{"name":"The Alfred Medical Research and Education Precinct","place":["Australia"]},{"name":"The University of Melbourne","place":["Australia"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2015,6,1]]},"reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/0165-4608(92)90043-8"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1158\/1078-0432.CCR-13-2575"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/leu.2012.339"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1158\/1541-7786.MCR-08-0167"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2004-02-0749"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1158\/0008-5472.CAN-05-0972"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.7314\/APJCP.2014.15.11.4555"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.canlet.2008.05.024"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1038\/onc.2010.561"},{"key":"e_1_3_2_11_2","first-page":"6629","article-title":"Effect of recombinant alpha-interferon on the expression of the bcr-abl fusion gene in human chronic myelogenous human leukemia cell lines","volume":"47","author":"Andrews DF","year":"1987","unstructured":"Andrews DF3rd, , Singer JW, , and Collins SJ. 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