{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T13:02:26Z","timestamp":1790946146054,"version":"4.1.0"},"reference-count":131,"publisher":"MDPI AG","issue":"20","license":[{"start":{"date-parts":[[2022,10,14]],"date-time":"2022-10-14T00:00:00Z","timestamp":1665705600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm initiated by the presence of the fusion gene BCR::ABL1. The development of tyrosine kinase inhibitors (TKIs) highly specific to p210BCR-ABL1, the constitutively active tyrosine kinase encoded by BCR::ABL1, has greatly improved the prognosis for CML patients. Now, the survival rate of CML nearly parallels that of age matched controls. However, therapy resistance remains a persistent problem in the pursuit of a cure. TKI resistance can be attributed to both BCR::ABL1 dependent and independent mechanisms. Recently, the role of non-coding RNAs (ncRNAs) has been increasingly explored due to their frequent dysregulation in a variety of malignancies. Specifically, microRNAs (miRNAs), circular RNAs (circRNAs), and long non-coding RNAs (lncRNAs) have been shown to contribute to the development and progression of therapy resistance in CML. Since each ncRNA exhibits multiple functions and is capable of controlling gene expression, they exert their effect on CML resistance through a diverse set of mechanisms and pathways. In most cases ncRNAs with tumor suppressing functions are silenced in CML, while those with oncogenic properties are overexpressed. Here, we discuss the relevance of many aberrantly expressed ncRNAs and their effect on therapy resistance in CML.<\/jats:p>","DOI":"10.3390\/ijms232012271","type":"journal-article","created":{"date-parts":[[2022,10,17]],"date-time":"2022-10-17T02:29:46Z","timestamp":1665973786000},"page":"12271","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Non-Coding RNAs Are Implicit in Chronic Myeloid Leukemia Therapy Resistance"],"prefix":"10.3390","volume":"23","author":[{"given":"Alexander","family":"Rudich","sequence":"first","affiliation":[{"name":"Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ramiro","family":"Garzon","sequence":"additional","affiliation":[{"name":"Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adrienne","family":"Dorrance","sequence":"additional","affiliation":[{"name":"Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2022,10,14]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"290","DOI":"10.1038\/243290a0","article-title":"Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining","volume":"243","author":"Rowley","year":"1973","journal-title":"Nature"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"100825","DOI":"10.1016\/j.blre.2021.100825","article-title":"Chronic Myeloid Leukemia: Modern therapies, current challenges and future directions","volume":"49","author":"Osman","year":"2021","journal-title":"Blood Rev."},{"key":"ref_3","doi-asserted-by":"crossref","first-page":"212","DOI":"10.1126\/science.3460176","article-title":"The Chronic Myelogenous Leukemia Specific P210-Protein Is the Product of the Bcr\/Abl Hybrid Gene","volume":"233","author":"Daley","year":"1986","journal-title":"Science"},{"key":"ref_4","doi-asserted-by":"crossref","first-page":"239","DOI":"10.1038\/306239a0","article-title":"Localization of the C-Abl Oncogene Adjacent to a Translocation Break Point in Chronic Myelocytic-Leukemia","volume":"306","author":"Heisterkamp","year":"1983","journal-title":"Nature"},{"key":"ref_5","doi-asserted-by":"crossref","first-page":"277","DOI":"10.1038\/306277a0","article-title":"Translocation of C-Abl Oncogene Correlates with the Presence of a Philadelphia-Chromosome in Chronic Myelocytic-Leukemia","volume":"306","author":"Bartram","year":"1983","journal-title":"Nature"},{"key":"ref_6","doi-asserted-by":"crossref","first-page":"93","DOI":"10.1016\/0092-8674(84)90077-1","article-title":"Philadelphia Chromosomal Breakpoints Are Clustered within a Limited Region, Bcr, on Chromosome-22","volume":"36","author":"Groffen","year":"1984","journal-title":"Cell"},{"key":"ref_7","doi-asserted-by":"crossref","first-page":"550","DOI":"10.1038\/315550a0","article-title":"Fused Transcript of Abl and Bcr Genes in Chronic Myelogenous Leukemia","volume":"315","author":"Shtivelman","year":"1985","journal-title":"Nature"},{"key":"ref_8","doi-asserted-by":"crossref","first-page":"1429","DOI":"10.1056\/NEJM198512053132301","article-title":"Evidence of a new chimeric bcr\/c-abl mRNA in patients with chronic myelocytic leukemia and the Philadelphia chromosome","volume":"313","author":"Stam","year":"1985","journal-title":"N. 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