scholarly journals RUNX3promoter hypermethylation is frequent in leukaemia cell lines and associated with acute myeloid leukaemia inv(16) subtype

2015 ◽  
Vol 169 (3) ◽  
pp. 344-351 ◽  
Author(s):  
Marcos R. H. Estécio ◽  
Sirisha Maddipoti ◽  
Carlos Bueso-Ramos ◽  
Courtney D. DiNardo ◽  
Hui Yang ◽  
...  
Keyword(s):  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Cell Lines ◽  
Leukaemia Cell ◽  
Acute Myeloid

scholarly journals Metabolomic Profiling of Drug Responses in Acute Myeloid Leukaemia Cell Lines

PLoS ONE ◽  
2009 ◽  
Vol 4 (1) ◽  
pp. e4251 ◽  
Author(s):  
Stefano Tiziani ◽  
Alessia Lodi ◽  
Farhat L. Khanim ◽  
Mark R. Viant ◽  
Christopher M. Bunce ◽  
...  
Keyword(s):  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Cell Lines ◽  
Leukaemia Cell ◽  
Drug Responses ◽  
Metabolomic Profiling ◽  
Acute Myeloid Leukaemia Cell ◽  
Acute Myeloid

Annexin II cell surface and mRNA expression in human acute myeloid leukaemia cell lines

2005 ◽  
Vol 115 (1-2) ◽  
pp. 109-114 ◽  
Author(s):  
Shane A. Olwill ◽  
Hugh McGlynn ◽  
William S. Gilmore ◽  
H. Denis Alexander
Keyword(s):  
Cell Surface ◽  
Acute Myeloid Leukaemia ◽  
Mrna Expression ◽  
Myeloid Leukaemia ◽  
Cell Lines ◽  
Annexin Ii ◽  
Leukaemia Cell ◽  
Acute Myeloid Leukaemia Cell ◽  
Acute Myeloid

scholarly journals Correction: Metabolomic Profiling of Drug Responses in Acute Myeloid Leukaemia Cell Lines

PLoS ONE ◽  
2009 ◽  
Vol 4 (4) ◽  
Author(s):  
Stefano Tiziani ◽  
Alessia Lodi ◽  
Farhat L. Khanim ◽  
Mark R. Viant ◽  
Christopher M. Bunce ◽  
...  
Keyword(s):  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Cell Lines ◽  
Leukaemia Cell ◽  
Drug Responses ◽  
Metabolomic Profiling ◽  
Acute Myeloid Leukaemia Cell ◽  
Acute Myeloid

scholarly journals p53 status of newly established acute myeloid leukaemia cell lines

1999 ◽  
Vol 79 (3-4) ◽  
pp. 407-415 ◽  
Author(s):  
A Zheng ◽  
K Castren ◽  
M Säily ◽  
E-R Savolainen ◽  
P Koistinen ◽  
...  
Keyword(s):  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Cell Lines ◽  
Leukaemia Cell ◽  
P53 Status ◽  
Acute Myeloid Leukaemia Cell ◽  
Acute Myeloid

scholarly journals Differences between intrinsic and acquired nucleoside analogue resistance in acute myeloid leukaemia cells

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Tamara Rothenburger ◽  
Dominique Thomas ◽  
Yannick Schreiber ◽  
Paul R. Wratil ◽  
Tamara Pflantz ◽  
...  
Keyword(s):  
Acute Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Cell Lines ◽  
Nucleoside Analogue ◽  
Acquired Resistance ◽  
Nucleoside Analogues ◽  
Cross Resistance ◽  
Enzymatic Assays ◽  
Anti Cancer ◽  
Acute Myeloid

Abstract Background SAMHD1 mediates resistance to anti-cancer nucleoside analogues, including cytarabine, decitabine, and nelarabine that are commonly used for the treatment of leukaemia, through cleavage of their triphosphorylated forms. Hence, SAMHD1 inhibitors are promising candidates for the sensitisation of leukaemia cells to nucleoside analogue-based therapy. Here, we investigated the effects of the cytosine analogue CNDAC, which has been proposed to be a SAMHD1 inhibitor, in the context of SAMHD1. Methods CNDAC was tested in 13 acute myeloid leukaemia (AML) cell lines, in 26 acute lymphoblastic leukaemia (ALL) cell lines, ten AML sublines adapted to various antileukaemic drugs, 24 single cell-derived clonal AML sublines, and primary leukaemic blasts from 24 AML patients. Moreover, 24 CNDAC-resistant sublines of the AML cell lines HL-60 and PL-21 were established. The SAMHD1 gene was disrupted using CRISPR/Cas9 and SAMHD1 depleted using RNAi, and the viral Vpx protein. Forced DCK expression was achieved by lentiviral transduction. SAMHD1 promoter methylation was determined by PCR after treatment of genomic DNA with the methylation-sensitive HpaII endonuclease. Nucleoside (analogue) triphosphate levels were determined by LC-MS/MS. CNDAC interaction with SAMHD1 was analysed by an enzymatic assay and by crystallisation. Results Although the cytosine analogue CNDAC was anticipated to inhibit SAMHD1, SAMHD1 mediated intrinsic CNDAC resistance in leukaemia cells. Accordingly, SAMHD1 depletion increased CNDAC triphosphate (CNDAC-TP) levels and CNDAC toxicity. Enzymatic assays and crystallisation studies confirmed CNDAC-TP to be a SAMHD1 substrate. In 24 CNDAC-adapted acute myeloid leukaemia (AML) sublines, resistance was driven by DCK (catalyses initial nucleoside phosphorylation) loss. CNDAC-adapted sublines displayed cross-resistance only to other DCK substrates (e.g. cytarabine, decitabine). Cell lines adapted to drugs not affected by DCK or SAMHD1 remained CNDAC sensitive. In cytarabine-adapted AML cells, increased SAMHD1 and reduced DCK levels contributed to cytarabine and CNDAC resistance. Conclusion Intrinsic and acquired resistance to CNDAC and related nucleoside analogues are driven by different mechanisms. The lack of cross-resistance between SAMHD1/ DCK substrates and non-substrates provides scope for next-line therapies after treatment failure.

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