Related LncRNAs
ID lncRNA Name Disease Method Sample Expression pattern Dysfunction type Description PMID Source
EL0289 CDKN2B-AS1 acute lymphoblastic leukemia MassARRAY assay etc. acute lymphoblastic leukemia tissue differential expression mutation rs564398 (A>G), mapping to the CDKN2BAS locus that encodes for ANRIL antisense non-coding RNA, showed a statistically significant correlation with the ALL phenotype, with a risk pattern that was compatible with an overdominant model of disease susceptibility. 21414664 LncRNADisease Lnc2Cancer
EL0289 CDKN2B-AS1 acute lymphoblastic leukemia N/A N/A N/A expression Higher p15AS levels were often found in acute lymphoblastic (ALL) and myeloid leukemias (AML). 21874119 LncRNADisease
EL0289 CDKN2B-AS1 acute lymphoblastic leukemia N/A N/A N/A expression Disruptions to the expression of ANRIL have accordingly been associated with the development of several cancer types, including neuroblastoma , acute lymphocytic leukaemia, melanoma and prostate 22817756 LncRNADisease
EL0289 CDKN2B-AS1 acute lymphoblastic leukemia qPCR, knockdown etc. cell lines (KG-1, Kasumi-1) up-regulated N/A We found an inverse relation between p15 antisense (p15AS) and p15 sense expression in leukaemia. A p15AS expression construct induced p15 silencing in cis and in trans through heterochromatin formation but not DNA methylation; the silencing persisted after p15AS was turned off, although methylation and heterochromatin inhibitors reversed this process. Moreover, 11 out of 16 patient samples (69%) showed relatively increased expression of p15AS and downregulated p15 expression (6/11 in acute myeloid leukaemia and 5/5 in acute lymphoblastic leukaemia). In contrast, 16 normal controls showed high expression of p15 but relatively low expression of the p15AS. Additionally, the two acute myeloid leukaemia lines, which displayed high p15AS and low p15 expression. 18185590 Lnc2Cancer
EL1049 PAWR acute lymphoblastic leukemia qPCR, Western blot, knockdown etc. T-ALL jurkat cell up-regulated N/A T-ALL-R-LncR1 was not observed in human normal tissues. However, an obvious expression was observed in some tumor tissues. T-ALL-R-LncR1 was markedly expressed in neoplastic T lymphocytes of 11 cases out of 21 children with T-ALL, indicating that T-ALL-R-LncR1 might be associated with T-ALL. T-ALL-R-LncR1 knockdown predisposed Jurkat cells to undergo pro-apoptotic factor Par-4-induced apoptosis. Further studies revealed that T-ALL-R-LncR1 knockdown facilitated the formation of a Par-4/THAP1 protein complex, resulting in the activation of caspase-3 and an increase of pro-apoptotic Smac protein in T-ALL cells 23906015 Lnc2Cancer