Childhood Acute Lymphoblastic Leukemia and Acute Non-Lymphoblastic Leukemia: Differences in Cellular Drug Resistance, with Emphasis on Glucocorticoids — A Pilot Study

Author(s):  
G. J. L. Kaspers ◽  
R. Pieters ◽  
C. H. Van Zantwijk ◽  
E. Klumper ◽  
K. Hählen ◽  
...  
2020 ◽  
Vol 27 (3) ◽  
pp. 385-392
Author(s):  
Zohreh Mousavi ◽  
Saeid Ghorbian ◽  
Azim Rezamand ◽  
Leyla Roshangar ◽  
Behboud Jafari

Background: Childhood acute lymphoblastic leukemia (ALL) explains 26% of pediatricmalignancies and is one of the leading causes of disease-related deaths in children. A novelmolecular class of non-coding genes, long non-coding RNAs (lncRNAs) having over 200nucleotides, have been defined as regulators of different cellular processes including pluripotency,oncogenesis, and transcription. It has been demonstrated that lncRNA transcription profilescan distinguish pre B-cell subtype of ALL accurately and act as early diagnostic and prognosticbiomarkers. Hence, the aim of this pilot study was the prior evaluation of expression profileof several lncRNA candidates including RP11-68I18.10, RP11-624C23.1, RP11-446E9, RP11-137H2.4, and RP11-203E8 in patients with ALL. Methods: In this study, 80 blood samples were obtained from patients, definitely diagnosed bypathologists with ALL, and from healthy subjects. Total RNA was extracted from blood samples,and cDNA was synthesized. Real-time PCR was applied to determine the expression of lncRNAs.A P-value of 0.010 was considered statistically significant. Results: Our findings revealed that the expression levels of lncRNAs RP11-624C23.1, RP11-446E9, RP11-137H2.4, RP11-68I18.10, and RP11-203E8 were significantly decreased in ALLsamples compared to those of healthy samples (P<0.0001, P =0.0616, P =0.0292, P<0.0001, andP = 0.0007). Moreover, the relationship between these five lncRNA expression changes and theimmunophenotype in ALL patients was not significant. Conclusion: The dysregulation of lncRNAs in ALL samples could provide a novel and interestingpossibility for early diagnosis and prognosis, as well as mastering the treatment of ALL.


Oncotarget ◽  
2015 ◽  
Vol 6 (40) ◽  
pp. 43048-43064 ◽  
Author(s):  
Jizhong Liu ◽  
Ashish Masurekar ◽  
Suzanne Johnson ◽  
Sohini Chakraborty ◽  
John Griffiths ◽  
...  

Blood ◽  
2005 ◽  
Vol 106 (5) ◽  
pp. 1817-1823 ◽  
Author(s):  
Amy Holleman ◽  
Monique L. den Boer ◽  
Karin M. Kazemier ◽  
H. Berna Beverloo ◽  
Anne R. M. von Bergh ◽  
...  

Abstract Drug resistance in childhood acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) is associated with impaired ability to induce apoptosis. To elucidate causes of apoptotic defects, we studied the protein expression of Apaf-1, procaspases-2, -3, -6, -7, -8, -10, and poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP) in cells from children with acute lymphoblastic leukemia (ALL; n = 43) and acute myeloid leukemia (AML; n = 10). PARP expression was present in all B-lineage samples, but absent in 4 of 15 T-lineage ALL samples and 3 of 10 AML cases, which was not caused by genomic deletions. PARP expression was a median 7-fold lower in T-lineage ALL (P &lt; .001) and 10-fold lower in AML (P &lt; .001) compared with B-lineage ALL. PARP expression was 4-fold lower in prednisolone, vincristine and L-asparaginase (PVA)-resistant compared with PVA-sensitive ALL patients (P &lt; .001). Procaspase-2 expression was 3-fold lower in T-lineage ALL (P = .022) and AML (P = .014) compared with B-lineage ALL. In addition, procaspase-2 expression was 2-fold lower in PVA-resistant compared to PVA-sensitive ALL patients (P = .042). No relation between apoptotic protease-activating factor 1 (Apaf-1), procaspases-3, -6, -7, -8, -10, and drug resistance was found. In conclusion, low baseline expression of PARP and procaspase-2 is related to cellular drug resistance in childhood acute lymphoblastic leukemia. (Blood. 2005;106:1817-1823)


2012 ◽  
Vol 53 (8) ◽  
pp. 1536-1542 ◽  
Author(s):  
Shih-Hsiang Chen ◽  
Chao-Ping Yang ◽  
Tang-Her Jaing ◽  
Iou-Jih Hung ◽  
Lee-Yung Shih ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document