Kirtonia, AnuradhaAshrafizadeh, MiladHushmandi, KiavashZabolian, AmirhosseinBejandi, Atefe K.Rani, ReshmaPandey, Amit K.Baligar, PrakashKumar, VinitDas, Bhudev C.Garg, Manoj2022-01-282022-01-282021Kirtonia A, Ashrafizadeh M, Zarrabi A, Hushmandi K, Zabolian A, Bejandi AK, Rani R, Pandey AK, Baligar P, Kumar V, Das BC, Garg M. Long noncoding RNAs: A novel insight in the leukemogenesis and drug resistance in acute myeloid leukemia. J Cell Physiol. 2021 Sep 27.https://doi.org/10.1002/jcp.30590https://hdl.handle.net/20.500.12713/2436Acute myeloid leukemia (AML) is a common hematological disorder with heterogeneous nature that resulted from blocked myeloid differentiation and an enhanced number of immature myeloid progenitors. During several decades, different factors, including cytogenetic, genetic, and epigenetic have been reported to contribute to the pathogenesis of AML by inhibiting the differentiation and ensuring the proliferation of myeloid blast cells. Recently, long noncoding RNAs (lncRNAs) have been considered as potential diagnostic, therapeutic, and prognostic factors in different human malignancies including AML. Altered expression of lncRNAs is correlated with the transformation of hematopoietic stem and progenitor cells into leukemic blast cells because of their distinct role in the key cellular processes. We discuss the significant role of lncRNAs in the proliferation, survival, differentiation, leukemic stem cells in AML and their involvement in different molecular pathways (insulin-like growth factor type I receptor, FLT3, c-KIT, Wnt, phosphatidylinositol 3-kinase/protein kinase-B, microRNAs), and associated mechanisms such as autophagy, apoptosis, and glucose metabolism. In addition, we aim to highlight the role of lncRNAs as reliable biomarkers for diagnosis, prognosis, and drug resistance for precision medicine in AML.eninfo:eu-repo/semantics/closedAccessAcute Myeloid LeukemiaChemoresistanceDifferentiationLong Noncoding RNAProliferationReview Article34569616WOS:0007000820000012-s2.0-85115666147Q1 - Q210.1002/jcp.30590N/A