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