{"title":"非编码rna对慢性粒细胞白血病伊马替尼耐药的影响","authors":"Fatemeh Ensafi Talemi , Soudeh Ghafouri-Fard","doi":"10.1016/j.lrr.2025.100529","DOIUrl":null,"url":null,"abstract":"<div><div>Imatinib is approved as the first-line treatment for newly diagnosed chronic myelogenous leukemia (CML). In spite of profound response in the majority of patients, resistance occurs in a subgroup of CML cases. Recently, it has been demonstrated that different classes of non-coding RNAs can modulate response to this tyrosine kinase inhibitor. Recognition of the role of these transcripts in this process not only expands our knowledge about the molecular mechanisms of imatinib resistance, but also provides novel strategies for combating this phenotype. The current review summarizes the role of non-coding RNAs in this process and suggests novel candidates for further studies in this field to enhance therapeutic response to imatinib.</div></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"24 ","pages":"Article 100529"},"PeriodicalIF":0.9000,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Impact of non-coding RNAs on resistance to imatinib in chronic myelogenous leukemia\",\"authors\":\"Fatemeh Ensafi Talemi , Soudeh Ghafouri-Fard\",\"doi\":\"10.1016/j.lrr.2025.100529\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Imatinib is approved as the first-line treatment for newly diagnosed chronic myelogenous leukemia (CML). In spite of profound response in the majority of patients, resistance occurs in a subgroup of CML cases. Recently, it has been demonstrated that different classes of non-coding RNAs can modulate response to this tyrosine kinase inhibitor. Recognition of the role of these transcripts in this process not only expands our knowledge about the molecular mechanisms of imatinib resistance, but also provides novel strategies for combating this phenotype. The current review summarizes the role of non-coding RNAs in this process and suggests novel candidates for further studies in this field to enhance therapeutic response to imatinib.</div></div>\",\"PeriodicalId\":38435,\"journal\":{\"name\":\"Leukemia Research Reports\",\"volume\":\"24 \",\"pages\":\"Article 100529\"},\"PeriodicalIF\":0.9000,\"publicationDate\":\"2025-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Leukemia Research Reports\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2213048925000317\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"HEMATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Leukemia Research Reports","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2213048925000317","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"HEMATOLOGY","Score":null,"Total":0}
Impact of non-coding RNAs on resistance to imatinib in chronic myelogenous leukemia
Imatinib is approved as the first-line treatment for newly diagnosed chronic myelogenous leukemia (CML). In spite of profound response in the majority of patients, resistance occurs in a subgroup of CML cases. Recently, it has been demonstrated that different classes of non-coding RNAs can modulate response to this tyrosine kinase inhibitor. Recognition of the role of these transcripts in this process not only expands our knowledge about the molecular mechanisms of imatinib resistance, but also provides novel strategies for combating this phenotype. The current review summarizes the role of non-coding RNAs in this process and suggests novel candidates for further studies in this field to enhance therapeutic response to imatinib.
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