{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T08:30:30Z","timestamp":1789547430808,"version":"build-2803163510"},"reference-count":93,"publisher":"MDPI AG","issue":"11","license":[{"start":{"date-parts":[[2015,11,18]],"date-time":"2015-11-18T00:00:00Z","timestamp":1447804800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"National Science Center, Poland","award":["2011\/03\/B\/NZ2\/01396"],"award-info":[{"award-number":["2011\/03\/B\/NZ2\/01396"]}]},{"name":"Medical University of Lodz, Poland","award":["03\/2-043-01\/50321001"],"award-info":[{"award-number":["03\/2-043-01\/50321001"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Genomic instability is a common feature of cancer cells, which can result from aberrant DNA damage reaction (DDR). We and others showed that the well-known BCR-ABL1 fusion oncogene, the cause of chronic myeloid leukemia, induced an increased production of reactive oxygen species (ROS) and conferred therapeutic drug resistance by suppression of apoptotic signaling, prolonged G2\/M arrest and stimulation of several pathways of DNA repair. However, to protect from apoptosis, cancer cells may tolerate some DNA lesions, which may increase genomic instability. Moreover, BCR\/ABL1-stimulated DNA repair might be faulty, especially non-homologous end joining in its alternative forms. Normal DNA repair can remove DNA damage and prevent mutations, reducing genome instability, but on the other hand, due to its imprecise nature, it may increase genomic instability by increasing the ratio of mutagenic DNA lesions. The example of BCR-ABL1-expressing cells shows that DNA repair can both increase and decrease genomic instability of cancer cells and understanding the mechanism of the regulation of these opposite effects would be helpful in anticancer strategies.<\/jats:p>","DOI":"10.3390\/ijms161126049","type":"journal-article","created":{"date-parts":[[2015,11,18]],"date-time":"2015-11-18T10:35:12Z","timestamp":1447842912000},"page":"27535-27549","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":28,"title":["DNA Repair\u2014A Double-Edged Sword in the Genomic Stability of Cancer Cells\u2014The Case of Chronic Myeloid Leukemia"],"prefix":"10.3390","volume":"16","author":[{"given":"Elzbieta","family":"Pawlowska","sequence":"first","affiliation":[{"name":"Department of Orthodontics, Medical University of Lodz, 92-216 Lodz, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janusz","family":"Blasiak","sequence":"additional","affiliation":[{"name":"Department of Molecular Genetics, University of Lodz, 90-236 Lodz, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2015,11,18]]},"reference":[{"key":"ref_1","first-page":"2049","article-title":"BCR-ABL tyrosine kinase activity regulates the expression of multiple genes implicated in the pathogenesis of chronic myeloid leukemia","volume":"60","author":"Deininger","year":"2000","journal-title":"Cancer Res."},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"6","DOI":"10.1186\/1756-8722-4-6","article-title":"BCR-ABL1-independent PI3Kinase activation causing imatinib-resistance","volume":"4","author":"Quentmeier","year":"2011","journal-title":"J. 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