{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T16:32:08Z","timestamp":1790526728770,"version":"4.1.0"},"reference-count":0,"publisher":"Frontiers Media SA","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Acta Biochim Pol"],"abstract":"<jats:p>Chronic myeloid leukemia (CML) results from the t(9;22) reciprocal chromosomal translocation producing the BCR-ABL1 gene, conferring growth and proliferation advantages in the CML cells. \u00a0CML progresses from chronic, often syndrome-free, to blast phase, fatal if not treated. Although the involvement of BCR-ABL1 in some signaling pathways is considered as the cause of CML, the mechanisms resulting in its progression are not completely known. However, BCR-ABL1 stimulates the production of reactive oxygen species (ROS), which levels increase with CML progression and induce BCR-ABL1 self-mutagenesis. Introducing imatinib and other tyrosine kinase inhibitors (TKIs) to CML therapy radically improved its outcome, but TKIs-resistance became an emerging problem. TKI-resistance can be associated with even higher ROS production than in TKI-sensitive cells. Therefore, ROS-induced self-mutagenesis of BCR-ABL1 can be crucial for CML progression and TKI resistance and in this way should be taken into account in therapeutic strategies. As a continuous production of ROS by BCR-ABL1 would lead to its self-destruction and death of CML cells, there must be mechanisms controlling this phenomenon. These can be dependent on DNA repair, which is modulated by BCR-ABL1 and can be different in CML stem and progenitor cells. Altogether, the mechanisms of the involvement of BCR-ABL1 in ROS signaling can be involved in CML progression and TKI-resistance and warrant further study.<\/jats:p>","DOI":"10.18388\/abp.2016_1396","type":"journal-article","created":{"date-parts":[[2016,12,1]],"date-time":"2016-12-01T06:58:06Z","timestamp":1480575486000},"source":"Crossref","is-referenced-by-count":11,"title":["Reactive oxygen species in BCR-ABL1-expressing cells \u2013 relevance to chronic myeloid leukemia"],"prefix":"10.3389","volume":"64","author":[{"given":"Joanna","family":"Antoszewska-Smith","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elzbieta","family":"Pawlowska","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janusz","family":"B\u0142asiak","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2016,12,1]]},"container-title":["Acta Biochimica Polonica"],"original-title":[],"link":[{"URL":"https:\/\/ojs.ptbioch.edu.pl\/index.php\/abp\/article\/download\/1396\/168","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/ojs.ptbioch.edu.pl\/index.php\/abp\/article\/download\/1396\/168","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,29]],"date-time":"2024-05-29T13:52:56Z","timestamp":1716990776000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.frontierspartnerships.org\/articles\/10.18388\/abp.2016_1396\/pdf"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2016,12,1]]},"references-count":0,"journal-issue":{"issue":"1","published-online":{"date-parts":[[2017,3,21]]}},"URL":"https:\/\/doi.org\/10.18388\/abp.2016_1396","relation":{},"ISSN":["1734-154X","0001-527X"],"issn-type":[{"value":"1734-154X","type":"electronic"},{"value":"0001-527X","type":"print"}],"subject":[],"published":{"date-parts":[[2016,12,1]]}}}