You're using an outdated browser. Please upgrade to a modern browser for the best experience.
Submitted Successfully!
Thank you for your contribution! You can also upload a video entry or images related to this topic. For video creation, please contact our Academic Video Service.
Version Summary Created by Modification Content Size Created at Operation
1 Hua Naranmandura -- 1902 2022-05-16 13:25:48 |
2 format correct Nora Tang Meta information modification 1902 2022-05-17 10:16:28 | |
3 format correct Nora Tang Meta information modification 1902 2022-05-18 07:57:51 |

Video Upload Options

We provide professional Academic Video Service to translate complex research into visually appealing presentations. Would you like to try it?
No, upload directly Yes
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Naranmandura, H.; Maimaitiyiming, Y.; , . LncRNAs in ALL Classification, Pathogenesis and Treatment. Encyclopedia. Available online: https://encyclopedia.pub/entry/22973 (accessed on 21 December 2025).
Naranmandura H, Maimaitiyiming Y,  . LncRNAs in ALL Classification, Pathogenesis and Treatment. Encyclopedia. Available at: https://encyclopedia.pub/entry/22973. Accessed December 21, 2025.
Naranmandura, Hua, Yasen Maimaitiyiming,  . "LncRNAs in ALL Classification, Pathogenesis and Treatment" Encyclopedia, https://encyclopedia.pub/entry/22973 (accessed December 21, 2025).
Naranmandura, H., Maimaitiyiming, Y., & , . (2022, May 16). LncRNAs in ALL Classification, Pathogenesis and Treatment. In Encyclopedia. https://encyclopedia.pub/entry/22973
Naranmandura, Hua, et al. "LncRNAs in ALL Classification, Pathogenesis and Treatment." Encyclopedia. Web. 16 May, 2022.
LncRNAs in ALL Classification, Pathogenesis and Treatment
Edit
This entry is adapted from the peer-reviewed paper 10.3390/ijms23084442

The coding regions account for only a small part of the human genome, and the remaining vast majority of the regions generate large amounts of non-coding RNAs. Although non-coding RNAs do not code for any protein, they are suggested to work as either tumor suppressers or oncogenes through modulating the expression of genes and functions of proteins at transcriptional, posttranscriptional and post-translational levels. Acute Lymphoblastic Leukemia (ALL) originates from malignant transformed B/T-precursor-stage lymphoid progenitors in the bone marrow (BM). The pathogenesis of ALL is closely associated with aberrant genetic alterations that block lymphoid differentiation and drive abnormal cell proliferation as well as survival. While treatment of pediatric ALL represents a major success story in chemotherapy-based elimination of a malignancy, adult ALL remains a devastating disease with relatively poor prognosis. Thus, novel aspects in the pathogenesis and progression of ALL, especially in the adult population, need to be further explored. Accumulating evidence indicated that genetic changes alone are rarely sufficient for development of ALL. Recent advances in cytogenic and sequencing technologies revealed epigenetic alterations including that of non-coding RNAs as cooperating events in ALL etiology and progression, which might provide new options for managing the disease in the future.

acute lymphoblastic leukemia ALL long non-coding RNA lncRNA circular RNA

1. LncRNAs in ALL Classification and Diagnosis

According to a study by Melo et al., the lncRNA expression profile showed significant alterations between different leukemia types and different subtypes of the same leukemia including ALL[1]. Another study found T-ALL subtype-specific lncRNA expression profiles, suggesting the involvement of lncRNAs as cooperators or downstream effectors during the corresponding oncogene-mediated leukemogenesis[2]. Alterations in chromatin and DNA modification also affect lncRNA expression profiles. It is reported that lncRNAs methylation per base pair shows a distinct profile between ALL and normal B-cell lymphoid precursors as well as among three sub clusters of ALL cases[3]. In human B-ALL samples, it was found that the lncRNA expression profile also correlates with cytogenetic abnormalities[4]. Likewise, many other studies also revealed subtype-specific and/or relapse-specific lncRNA signatures in ALL patent samples[5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]. These studies suggest that lncRNAs are associated with the pathogenesis of ALL and might be used as molecular markers for disease classification and diagnosis.

2. LncRNAs as Cooperating Events of Genetic Abnormalities in T-ALL Pathogenesis

T-ALL patients have a worse prognosis than those with B-ALL probably due to the less-known and more complex mechanism on its etiology, maintenance, and progression[21][22], suggesting the importance of exploring novel aspects in the pathogenesis and progression of T-ALL. Zhang et al. found that a lncRNA named T-ALL-related long non-coding RNA (T-ALL-R-LncR1) is markedly expressed in T-ALL Jurkat cells and 50% of T-ALL patient primary cells[23]. Importantly, knockdown of T-ALL-R-LncR1 led to apoptosis in Jurkat cells[23]. This finding suggests that the lncRNA T-ALL-R-LncR1 confers resistance to apoptosis, playing an oncogenic role in T-ALL development. It is well demonstrated that T cell acute lymphocytic leukemia protein 1 (TAL1, also known as SCL) is one of the most prevalent oncogenic transcription factors in T-ALL[24][25]. Generally, TAL1 coordinates with other transcription factors including GATA3, RUNX1, and MYB to regulate the expression of their downstream target genes in T-ALL cells[26]. Interestingly, TAL1 reportedly activated a subset of lncRNAs, some of which are regulated by GATA3,RUNX1, and MYB in a coordinated manner[19]; another subset of lncRNAs negatively regulated by TAL1 were also identified. Notably, the transcription factors T-cell leukemia homeobox 1 (TLX1) and TLX3 are key drivers of the TLX1/NKX2.1 and TLX subgroups of T-ALL, respectively[24][27]. A study showed that TLX1 directly regulates a set of lncRNAs, some of which are marked by super-enhancers[20], indicating the involvement of lncRNAs in TLX1-induced gene expression regulation. Intriguingly, some lncRNAs give rise to other ncRNA types following further processing. It was reported that TLX3 binds and transactivates lncRNA LINC00478, which is the host of miR125-b, to regulate miR-125b production, through which supports growth and invasiveness of T-ALL cells[28]. Collectively, these findings suggest that lncRNAs are crucial downstream effectors of major genetic abnormalities in the pathogenesis of T-ALL.
T-ALL is driven by oncogenic transcription factors (e.g., LTX1, LTX3 or HOXA, and TAL/LMO) that act along with secondary acquired mutations[24][25]. For instance, NOTCH1 activating mutations are identified in more than 50% of T-ALL cases, suggesting a key role in driving the disease[29]. A study by Durinck et al. established a novel lncRNA network that acts downstream of NOTCH1 during normal and malignant thymocyte development[30], specifically, they identified 40 lncRNAs that are positively regulated by NOTCH1 in both normal and malignant T lymphocytes, supporting an important role for these lncRNAs as downstream effectors in NOTCH1-regulated T-cell biology. Another study also uncovered a set of T-ALL-specific lncRNAs, many of which are directly regulated by the NOTCH1/RPBJκ activator complex[5]; the authors showed that one specific NOTCH-regulated lncRNA, LUNAR1, is required for efficient T-ALL growth in vitro and in vivo due to its ability to enhance insulin-like growth factor 1 (IGF1) receptor (IGF1R) mRNA level and sustain IGF1 signaling. Likewise, a lncRNA named NALT, which is located only 100 bp away from NOTCH1 gene, was upregulated in human NOTCH1-activated T-ALL samples[31]; increased expression of NALT dramatically promoted cell proliferation, while knockdown of NALT caused the opposite effect; mechanistically, nuclear located NALT functioned as a transcription activator causing activation of the NOTCH1 signaling pathway.

3. LncRNAs as Cooperating Events of Genetic Abnormalities in B-ALL Pathogenesis

Fusion genes produced by chromosomal translocations are often strong oncogenic drivers and cytogenetic abnormalities in hematological malignancies such as acute myeloid leukemia (AML) or lymphoma[32][33]. Similarly, fusion oncogenes represent a prominent class of oncogenic drivers in ALL as well[21][34][35]. ETV6-RUNX1 generated by t(12;21) is the most common oncogenic fusion gene in childhood B-ALL[36]. A comprehensive analysis of the lncRNA transcriptome in ETV6-RUNX1+ B-ALL revealed the fusion protein-specific lncRNA expression signature[37]. Further analysis showed that expression of lncRNAs NKX2-3-1, TIMM21-5, ASTN1-1, and RTN4R-1 are linked to the oncogenic fusion protein. Knockdown of NKX2-3-1 and RTN4R-1 in ETV6-RUNX1+ cells reversed the expression of genes deregulated by the ETV6-RUNX1 fusion protein[37]. Likewise, lncRNA CASC15 is overexpressed in ETV6-RUNX1+ B-ALL, and shows increased expression of its chromosomally adjacent gene, SOX4, which encodes a transcriptional activator in lymphocytes, thereby upregulating cell survival, and proliferation[38]. An oncogenic lncRNA TCL6 was also upregulated in the ETV6-RUNX1+ B-ALL and probably associates with poor disease-free survival[9]. Collectively, these findings suggest the involvement of lncRNAs in fusion oncogene-mediated pathogenesis and progression of ALL.
Fusion of the mixed lineage leukemia (MLL) gene with other partner genes are common in pediatric leukemias, and MLL-rearranged B-ALL has long been considered a refractory disease due to the poor prognosis of associated patients[39]. A genome-wide lncRNA expression study found 52 upregulated and 59 downregulated lncRNAs between MLL-rearranged and MLL-unarranged ALL patient samples[40]; bioinformatics analysis showed that several lncRNAs correspond to the expression of the MLL fusion protein partner genes, such as HOXA and MEIS1 among others, and some other lncRNAs are associated with histone-related functions or membrane proteins; further, three subtypes of MLL rearranged ALL (MLL-AF4+, MLL-AF9+, and MLL-ENL+) showed a translocation specific lncNRA expression signature[40]. Another study reported that lncRNA BALR-6 is highly expressed in MLL-rearranged patient samples[41]; knockdown of BALR-6 reduced cell proliferation and induced apoptosis, while overexpression of BALR-6 caused a significant increase in early hematopoietic progenitor populations in murine BM transplantation experiments, suggesting that its dysregulation may cause developmental changes.

4. LncRNAs and Immune Response Modulation in ALL Pathogenesis and Treatment

The immune suppressive tumor microenvironment is proven essential in the pathogenesis of many cancer types[42][43][44]. LncRNAs NONHSAT027612.2 and NONHSAT134556.2 were significantly elevated in the blood and bone marrow (BM) of pediatric ALL patients, and may serve important roles in the pathogenesis of childhood ALL via suppressing immune response-associated pathways[11]. Besides, in the BM of patients with childhood T-ALL, membrane-localized and cytoplasm-localized lncRNA insulin receptor precursor (INSR) promoted CD4+ regulatory T-cell distribution and decreased the percentage of CD8+ cytotoxic T-cells in the BM of pediatric T-ALL patients, facilitating leukemic cell growth via immune suppression[45]. Mechanistically, through direct binding with INSR protein, lncRNA-INSR blocked the INSR ubiquitination site, causing abnormal accumulation and activation of INSR and the PI3K/AKT-signaling pathway. LncRNAs are also implicated in CART therapy of B-ALL[46]; specifically, a set of lncRNAs showed high degree of co-expression with transcription factors or histones (i.e., FOS and HIST1H4B) and were associated with immune processes during CAR-T therapy of B-ALL. These findings suggest that lncRNAs are important players in the immune response regulation in ALL pathogenesis and treatment.

5. LncRNAs in Susceptibility, Treatment Response and Prognosis of ALL

Single nucleotide polymorphism (SNP) is common in the human genome, and has profound implications in the pathogenesis/susceptibility of varying diseases. It was reported that the rs2147578 polymorphism of lncRNA LAMC2-1 may be a risk factor for developing childhood ALL, suggesting that SNPs might confer oncogenic properties on lncRNAs[47]. LncRNA PAX8-AS1 is located in the upstream region of PAX8, a gene encodes the transcription factor PAX8 required for cell growth and differentiation during embryonic development, and potentially regulates PAX8 expression[48]. Similarly, Bahari et al. reported that polymorphisms rs4848320 and rs6726151 of PAX8-AS1 might be risk factors for the development of childhood ALL[49]. Also, rs7158663 AG/AA genotypes of lncRNA MEG3 were associated with higher susceptibility to childhood ALL[50]. These findings indicate that some SNPs on lncRNAs are indicative of higher susceptibility for developing ALL.
Fernando et al. reported a correlation of high lncRNA BALR-2 expression with the diminished response to prednisone treatment and poor survival in patients[4]. BALR-2 knockdown led to reduced proliferation, increased apoptosis, as well as augmented sensitivity to prednisone treatment via activation of the glucocorticoid (GC) response pathway in both human and mouse B cells[4]. Another study reported that five lncRNAs are specifically upregulated in childhood B-ALL, and these lncRNAs had significant impacts on cell proliferation, migration, apoptosis, and treatment response[51]. In particular, expression of lncRNA RP11-137H2.4 was negatively associated with GC response[51]. Similarly, lncRNA GAS5 was also found to be a potential marker of GC response in remission induction therapy of childhood ALL[52]. A high expression of the lncRNA CDKN2B-AS1 level was associated with Adriamycin resistance[53]. Gioia et al. reported that LncRNAs RP11-624C23.1 and RP11-203E8 were downregulated in ALL, and restoring their expression in ALL cells’ increased sensitivity to genotoxic stress (e.g., chemotherapy agents), possibly by modulating the DNA damage response pathway[54]. These studies suggest that lncRNAs are important indicators of treatment response in ALL therapy.
Due to the strong oncogenic roles, some lncRNAs might predict prognosis in ALL patients. For example, lncRNA ZEB1-AS1 promoted the activation of IL-11/STAT3 signaling pathway by interacting with IL-11 in B-ALL cells, and a high expression of lncRNA ZEB1-AS1 predicted a poor prognosis for B-ALL patients[38]. A bioinformatics analysis presented a lncRNA-mRNA-based classifier that might be clinically useful to predict the recurrence and prognosis for childhood ALL[55]. It is also reported that the lncRNAs NEAT1 and MALAT1 sponges miR-335-3p, increasing the multidrug-resistance gene ATP-binding cassette sub-family A member 3 (ABCA3) expression and leading to poor prognosis in childhood ALL[56]. Many other studies also found similar roles of lncRNAs in prediction of the prognosis in ALL patients[36][49][57][58][59][60][61][62].
In conclusion, alterations in the expression of lncRNAs are important cooperating events in ALL pathogenesis, maintenance, and progression. Therefore, lncRNAs could be applied in diagnosis, classification, risk stratification, prognosis, as well as treatment of ALL.

References

  1. Melo CP, Campos CB, Rodrigues Jde O, et al. Long non-coding RNAs: biomarkers for acute leukaemia subtypes. Br J Haematol. 2016;173(2):318-320.
  2. Wallaert A, Durinck K, Van Loocke W, et al. Long noncoding RNA signatures define oncogenic subtypes in T-cell acute lymphoblastic leukemia. Leukemia. 2016;30(9):1927-1930.
  3. Arthur G, Almamun M, Taylor K. Hypermethylation of antisense long noncoding RNAs in acute lymphoblastic leukemia. Epigenomics. 2017;9(5):635-645.
  4. Fernando TR, Rodriguez-Malave NI, Waters EV, et al. LncRNA Expression Discriminates Karyotype and Predicts Survival in B-Lymphoblastic Leukemia. Mol Cancer Res. 2015;13(5):839-851.
  5. Trimarchi T, Bilal E, Ntziachristos P, et al. Genome-wide mapping and characterization of Notch-regulated long noncoding RNAs in acute leukemia. Cell. 2014;158(3):593-606.
  6. Cheng H, Huang CM, Wang Y, et al. Microarray profiling and co-expression network analysis of the lncRNAs and mRNAs associated with acute leukemia in adults. Mol Biosyst. 2017;13(6):1102-1108.
  7. Lajoie M, Drouin S, Caron M, et al. Specific expression of novel long non-coding RNAs in high-hyperdiploid childhood acute lymphoblastic leukemia. PLoS One. 2017;12(3):e0174124.
  8. Caron M, St-Onge P, Drouin S, et al. Very long intergenic non-coding RNA transcripts and expression profiles are associated to specific childhood acute lymphoblastic leukemia subtypes. PLoS One. 2018;13(11):e0207250.
  9. Cuadros M, Andrades Á, Coira IF, et al. Expression of the long non-coding RNA TCL6 is associated with clinical outcome in pediatric B-cell acute lymphoblastic leukemia. Blood Cancer J. 2019;9(12):93.
  10. James AR, Schroeder MP, Neumann M, et al. Long non-coding RNAs defining major subtypes of B cell precursor acute lymphoblastic leukemia. J Hematol Oncol. 2019;12(1):8.
  11. Li S, Bian H, Cao Y, et al. Identification of novel lncRNAs involved in the pathogenesis of childhood acute lymphoblastic leukemia. Oncol Lett. 2019;17(2):2081-2090.
  12. Affinito O, Pane K, Smaldone G, et al. lncRNAs-mRNAs Co-Expression Network Underlying Childhood B-Cell Acute Lymphoblastic Leukaemia: A Pilot Study. Cancers (Basel). 2020;12(9):2489.
  13. Bárcenas-López DA, Núñez-Enríquez JC, Hidalgo-Miranda A, et al. Transcriptome Analysis Identifies LINC00152 as a Biomarker of Early Relapse and Mortality in Acute Lymphoblastic Leukemia. Genes (Basel). 2020;11(3):302.
  14. Cuadros M, García DJ, Andrades A, et al. LncRNA-mRNA Co-Expression Analysis Identifies AL133346.1/CCN2 as Biomarkers in Pediatric B-Cell Acute Lymphoblastic Leukemia. Cancers (Basel). 2020;12(12):3803.
  15. Yu W, Wang W, Yu X. Investigation of lncRNA-mRNA co-expression network in ETV6-RUNX1-positive pediatric B-cell acute lymphoblastic leukemia. PLoS One. 2021;16(6):e0253012.
  16. das Chagas PF, de Sousa GR, Kodama MH, et al. Ultraconserved long non-coding RNA uc.112 is highly expressed in childhood T versus B-cell acute lymphoblastic leukemia. Hematol Transfus Cell Ther. 2021;43(1):28-34.
  17. Wang W, Lyu C, Wang F, et al. Identification of Potential Signatures and Their Functions for Acute Lymphoblastic Leukemia: A Study Based on the Cancer Genome Atlas. Front Genet. 2021;12:656042.
  18. Xia J, Wang M, Zhu Y, Bu C, Li T. Differential mRNA and long noncoding RNA expression profiles in pediatric B-cell acute lymphoblastic leukemia patients. BMC Pediatr. 2022;22(1):10.
  19. Ngoc PCT, Tan SH, Tan TK, et al. Identification of novel lncRNAs regulated by the TAL1 complex in T-cell acute lymphoblastic leukemia. Leukemia. 2018;32(10):2138-2151.
  20. Verboom K, Van Loocke W, Volders PJ, et al. A comprehensive inventory of TLX1 controlled long non-coding RNAs in T-cell acute lymphoblastic leukemia through polyA+ and total RNA sequencing. Haematologica. 2018;103(12):e585-e589.
  21. Malard F, Mohty M. Acute lymphoblastic leukaemia. Lancet. 2020;395(10230):1146-1162.
  22. Zheng S, Gillespie E, Naqvi AS, et al. Modulation of CD22 Protein Expression in Childhood Leukemia by Pervasive Splicing Aberrations: Implications for CD22-Directed Immunotherapies. Blood Cancer Discov. 2022;3(2):103-115.
  23. Zhang L, Xu HG, Lu C. A novel long non-coding RNA T-ALL-R-LncR1 knockdown and Par-4 cooperate to induce cellular apoptosis in T-cell acute lymphoblastic leukemia cells. Leuk Lymphoma. 2014;55(6):1373-1382.
  24. Cordo' V, van der Zwet JCG, Canté-Barrett K, Pieters R, Meijerink JPP. T-cell Acute Lymphoblastic Leukemia: A Roadmap to Targeted Therapies. Blood Cancer Discov. 2020;2(1):19-31.
  25. van der Zwet JCG, Cordo' V, Canté-Barrett K, Meijerink JPP. Multi-omic approaches to improve outcome for T-cell acute lym-phoblastic leukemia patients. Adv Biol Regul. 2019;74:100647.
  26. Sanda T, Lawton LN, Barrasa MI, et al. Core transcriptional regulatory circuit controlled by the TAL1 complex in human T cell acute lymphoblastic leukemia. Cancer Cell. 2012;22(2):209-221.
  27. Vanner RJ, Dobson SM, Gan OI, et al. Multiomic Profiling of Central Nervous System Leukemia Identifies mRNA Translation as a Therapeutic Target. Blood Cancer Discov. 2022;3(1):16-31.
  28. Renou L, Boelle PY, Deswarte C, et al. Homeobox protein TLX3 activates miR-125b expression to promote T-cell acute lymphoblastic leukemia. Blood Adv. 2017;1(12):733-747.
  29. Grabher C, von Boehmer H, Look AT. Notch 1 activation in the molecular pathogenesis of T-cell acute lymphoblastic leukaemia. Nat Rev Cancer. 2006;6(5):347-359.
  30. Durinck K, Wallaert A, Van de Walle I, et al. The Notch driven long non-coding RNA repertoire in T-cell acute lymphoblastic leukemia. Haematologica. 2014;99(12):1808-1816.
  31. Wang Y, Wu P, Lin R, Rong L, Xue Y, Fang Y. LncRNA NALT interaction with NOTCH1 promoted cell proliferation in pediatric T cell acute lymphoblastic leukemia. Sci Rep. 2015;5:13749.
  32. Maimaitiyiming Y, Wang QQ, Yang C, et al. Hyperthermia Selectively Destabilizes Oncogenic Fusion Proteins. Blood Cancer Discov. 2021;2(4):388-401.
  33. Renneville A, Gasser JA, Grinshpun DE, et al. Avadomide induces degradation of ZMYM2 fusion oncoproteins in hematologic malignancies. Blood Cancer Discov. 2021;2(3):250-265.
  34. Terwilliger T, Abdul-Hay M. Acute lymphoblastic leukemia: a comprehensive review and 2017 update. Blood Cancer J. 2017;7(6):e577.
  35. Tsuzuki S, Yasuda T, Kojima S, et al. Targeting MEF2D-fusion Oncogenic Transcriptional Circuitries in B-cell Precursor Acute Lymphoblastic Leukemia. Blood Cancer Discov. 2020;1(1):82-95.
  36. Montaño A, Ordoñez JL, Alonso-Pérez V, et al. ETV6/RUNX1 Fusion Gene Abrogation Decreases the Oncogenicity of Tumour Cells in a Preclinical Model of Acute Lymphoblastic Leukaemia. Cells. 2020;9(1):215.
  37. Ghazavi F, De Moerloose B, Van Loocke W, et al. Unique long non-coding RNA expression signature in ETV6/RUNX1-driven B-cell precursor acute lymphoblastic leukemia. Oncotarget. 2016;7(45):73769-73780.
  38. Wang Q, Du X, Yang M, et al. LncRNA ZEB1-AS1 contributes to STAT3 activation by associating with IL-11 in B-lymphoblastic leukemia. Biotechnol Lett. 2017;39(12):1801-1810.
  39. El Chaer F, Keng M, Ballen KK. MLL-Rearranged Acute Lymphoblastic Leukemia. Curr Hematol Malig Rep. 2020;15(2):83-89.
  40. Fang K, Han BW, Chen ZH, et al. A distinct set of long non-coding RNAs in childhood MLL-rearranged acute lymphoblastic leukemia: biology and epigenetic target. Hum Mol Genet. 2014;23(12):3278-3288.
  41. Wang X, Yang J, Guo G, et al. Novel lncRNA-IUR suppresses Bcr-Abl-induced tumorigenesis through regulation of STAT5-CD71 pathway. Mol Cancer. 2019;18(1):84.
  42. Becker JC, Andersen MH, Schrama D, Thor Straten P. Immune-suppressive properties of the tumor microenvironment. Cancer Immunol Immunother. 2013;62(7):1137-1148.
  43. Niesel K, Schulz M, Anthes J, et al. The immune suppressive microenvironment affects efficacy of radio-immunotherapy in brain metastasis. EMBO Mol Med. 2021;13(5):e13412.
  44. Haloupek N. The Landscape of Blood Cancer Research Today-and Where the Field Is Headed. Blood Cancer Discov. 2020;1(1):1-4.
  45. Wang Y, Yang X, Sun X, et al. Bone marrow infiltrated Lnc-INSR induced suppressive immune microenvironment in pediatric acute lymphoblastic leukemia. Cell Death Dis. 2018;9(10):1043.
  46. Zhang Q, Hu H, Chen SY, et al. Transcriptome and Regulatory Network Analyses of CD19-CAR-T Immunotherapy for B-ALL. Genomics Proteomics Bioinformatics. 2019;17(2):190-200.
  47. Hashemi M, Bahari G, Naderi M, Sadeghi Bojd S, Taheri M. Association of lnc-LAMC2-1:1 rs2147578 and CASC8 rs10505477 Polymorphisms with Risk of Childhood Acute Lymphoblastic Leukemia. Asian Pac J Cancer Prev. 2016;17(11):4985-4989.
  48. Han J, Zhou W, Jia M, et al. Expression quantitative trait loci in long non-coding RNA PAX8-AS1 are associated with decreased risk of cervical cancer. Mol Genet Genomics. 2016;291(4):1743-1748.
  49. Bahari G, Hashemi M, Naderi M, Sadeghi-Bojd S, Taheri M. Long non-coding RNA PAX8-AS1 polymorphisms increase the risk of childhood acute lymphoblastic leukemia. Biomed Rep. 2018;8(2):184-190.
  50. Pei JS, Chang WS, Chen CC, et al. Novel Contribution of Long Non-coding RNA MEG3 Genotype to Prediction of Childhood Leukemia Risk. Cancer Genomics Proteomics. 2022;19(1):27-34.
  51. Ouimet M, Drouin S, Lajoie M, et al. A childhood acute lymphoblastic leukemia-specific lncRNA implicated in prednisolone resistance, cell proliferation, and migration. Oncotarget. 2017;8(5):7477-7488.
  52. Gasic V, Stankovic B, Zukic B, et al. Expression Pattern of Long Non-coding RNA Growth Arrest-specific 5 in the Remission Induction Therapy in Childhood Acute Lymphoblastic Leukemia. J Med Biochem. 2019;38(3):292-298.
  53. Chen L, Shi Y, Li J, et al. LncRNA CDKN2B-AS1 contributes to tumorigenesis and chemoresistance in pediatric T-cell acute lymphoblastic leukemia through miR-335-3p/TRAF5 axis. Anticancer Drugs. 2020;10.1097/CAD.0000000000001001.
  54. Gioia R, Drouin S, Ouimet M, et al. LncRNAs downregulated in childhood acute lymphoblastic leukemia modulate apoptosis, cell migration, and DNA damage response. Oncotarget. 2017;8(46):80645-80650.
  55. Qi H, Chi L, Wang X, Jin X, Wang W, Lan J. Identification of a Seven-lncRNA-mRNA Signature for Recurrence and Prognostic Prediction in Relapsed Acute Lymphoblastic Leukemia Based on WGCNA and LASSO Analyses. Anal Cell Pathol (Amst). 2021;2021:6692022.
  56. Pouyanrad S, Rahgozar S, Ghodousi ES. Dysregulation of miR-335-3p, targeted by NEAT1 and MALAT1 long non-coding RNAs, is associated with poor prognosis in childhood acute lymphoblastic leukemia. Gene. 2019;692:35-43.
  57. El-Khazragy N, Abdel Aziz MA, Hesham M, et al. Upregulation of leukemia-induced non-coding activator RNA (LUNAR1) predicts poor outcome in pediatric T-acute lymphoblastic leukemia. Immunobiology. 2021;226(6):152149.
  58. Zeng P, Chai Y, You C, et al. Correlation analysis of long non-coding RNA TUG1 with disease risk, clinical characteristics, treatment response, and survival profiles of adult Ph- Acute lymphoblastic leukemia. J Clin Lab Anal. 2021;35(8):e23583.
  59. Zhang YY, Huang SH, Zhou HR, Chen CJ, Tian LH, Shen JZ. Role of HOTAIR in the diagnosis and prognosis of acute leukemia. Oncol Rep. 2016;36(6):3113-3122.
  60. Chen Z, Yang F, Liu H, et al. Identification of a nomogram based on an 8-lncRNA signature as a novel diagnostic biomarker for childhood acute lymphoblastic leukemia. Aging (Albany NY). 2021;13(11):15548-15568.
  61. Gao W. Long non-coding RNA MEG3 as a candidate prognostic factor for induction therapy response and survival profile in childhood acute lymphoblastic leukemia patients. Scand J Clin Lab Invest. 2021;81(3):194-200.
  62. Xagorari M, Marmarinos A, Kossiva L, et al. Overexpression of the GR Riborepressor LncRNA GAS5 Results in Poor Treatment Response and Early Relapse in Childhood B-ALL. Cancers (Basel). 2021;13(23):6064.
  63. Xagorari M, Marmarinos A, Kossiva L, et al. Overexpression of the GR Riborepressor LncRNA GAS5 Results in Poor Treatment Response and Early Relapse in Childhood B-ALL. Cancers (Basel). 2021;13(23):6064.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Hematology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : Hua Naranmandura , Yasen Maimaitiyiming ,
View Times: 539
Revisions: 3 times (View History)
Update Date: 18 May 2022
Table of Contents
    Notice
    You are not a member of the advisory board for this topic. If you want to update advisory board member profile, please contact office@encyclopedia.pub.
    OK
    Confirm
    Only members of the Encyclopedia advisory board for this topic are allowed to note entries. Would you like to become an advisory board member of the Encyclopedia?
    Yes
    No
    ${ textCharacter }/${ maxCharacter }
    Submit
    Cancel
    There is no comment~
    ${ textCharacter }/${ maxCharacter }
    Submit
    Cancel
    ${ selectedItem.replyTextCharacter }/${ selectedItem.replyMaxCharacter }
    Submit
    Cancel
    Confirm
    Are you sure to Delete?
    Yes No
    Academic Video Service
    Feedback