作者: María Sol Ruiz , María Belén Sánchez , Simone Bonecker , Carolina Furtado , Daniel Koile
DOI: 10.1101/2020.03.16.989194
关键词:
摘要: Chronic myeloid leukemia (CML) is a stem cell neoplasm characterized by an expansion of progenitor cells and the presence BCR-ABL1 oncoprotein. Since introduction specific tyrosine kinase inhibitors (TKI), overall survival has improved significantly. However, under long-term therapy patients may have residual disease that originates from TKI-resistant leukemic (LSC). In this work, we analyzed miRNome CML LSC, normal hematopoietic (HSC) obtained same patients, healthy donors (HD) next-generation sequencing. We detected global decrease microRNA levels in LSC HSC decreased microRNAs snoRNAs imprinted genomic cluster chromosome 14, suggesting mechanism silencing multiple non-coding RNAs. Surprisingly, despite absence expression, showed altered miRNome. silico analysis revealed association between validated metabolic pathways, these molecules be mediators previously reported dysregulation metabolism. This first report distinguishes BCR-ABL1+ vs. their BCR-ABL1- counterparts, providing valuable data for future studies.