scholarly journals Successful resolution of hemophagocytic lymphohistiocytosis during the chemotherapy course of acute myelocytic leukemia with ruxolitinib

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Yue Song ◽  
Jing-Shi Wang ◽  
Xin-Kai Wang ◽  
Yi-Ni Wang ◽  
Zhao Wang
2016 ◽  
Vol 91 (1) ◽  
pp. 79-83
Author(s):  
Jung A Yoon ◽  
Min Kyung Jeon ◽  
Sun-myoung Kang ◽  
Eunhye Oh ◽  
Seung Hwan Shin ◽  
...  

Blood ◽  
1968 ◽  
Vol 32 (4) ◽  
pp. 507-523 ◽  
Author(s):  
ROSE RUTH ELLISON ◽  
JAMES F. HOLLAND ◽  
MARISE WEIL ◽  
CLAUDE JACQUILLAT ◽  
MICHEL BOIRON ◽  
...  

Abstract Arabinosyl cytosine (ara-C), a synthetic pyrimidine nucleoside related to the normal metabolites cytidine and deoxycytidine, has been found capable of producing marrow remission at tolerable doses in acute myelocytic and acute lymphocytic leukemia in adults. There were 16 per cent remissions complete in all aspects, 3 per cent complete except for hemoglobin level, and 6 per cent partial remissions among 180 adults with acute myelocytic leukemia treated with any one of 8 variants of infusion duration or daily dose of ara-C. Twenty-four per cent of 37 adults with acute lymphocytic or unclassified leukemia had complete or partial remissions. The comparison of 1, 4, 12 and 24 hours infusion of ara-C (to total dose tolerated) does not show significant superiority for any one group. The complete remission rate with 1 or 12 hour infusions, however, is 25 per cent (superior to that obtained with 6-mercaptopurine) and the recommended schedule of treatment for ara-C based on these data is, therefore, daily infusions of 100 or 50 mg./m.2 in one hour for approximately 3 to 6 weeks followed by maintenance therapy of once weekly subcutaneous injection of 30 mg./m.2 of ara-C. Platelet transfusions should be available when ara-C is used.


2003 ◽  
Vol 140 (1) ◽  
pp. 13-17 ◽  
Author(s):  
Caterina Matteucci ◽  
Roberta La Starza ◽  
Barbara Crescenzi ◽  
Silvia Romoli ◽  
Alessandra Santoro ◽  
...  

2009 ◽  
Vol 30 (5) ◽  
pp. 671-673 ◽  
Author(s):  
Ankit Shrivastav ◽  
Varun Kumar ◽  
Jyotirmoy Pal

1979 ◽  
Vol 6 (3) ◽  
pp. 261-277 ◽  
Author(s):  
Peter H. Wiernik ◽  
Oliver J. Glidewell ◽  
H. Clark Hoagland ◽  
Kurt W. Brunner ◽  
Charles L. Spurr ◽  
...  

2021 ◽  
Vol 27 ◽  
Author(s):  
Jun Wu ◽  
Ming-Zhu Song ◽  
Li-Jun Deng ◽  
Qian-Ling Ye

Background: Epigenetic modifications have recently attracted much attention in the study of the biological mechanisms of acute myelocytic leukemia (AML) for therapy and prognosis. However, studies on DNA methylation changes during AML treatment are limited. Objective: The comprehensive DNA methylation-transcriptome profiles association analysis in this study aimed to establish whole-genome DNA methylation profiles and explore DNA methylation-related genes and their potential functions before and after treatment. And more appropriate biomarkers are expected to be identified for therapy strategies in AML. Method: Illumina 450K and RNA-Seq data were obtained from The Cancer Genome Atlas. We performed comprehensive DNA methylation-transcriptome profiles association analysis, pathway analysis, correlation analysis, and survival analyses. The StarBase database was utilized to predict interactions between lncRNAs, miRNAs and target mRNAs. Results: In total, 1592 distinct CpG sites and 2419 different expression transcripts were identified between pre-treatment and post-treatment AML. The significantly enriched functions of methylated genes were stem cell differentiation, cell population maintenance, and cell development. The expression of UGT3A2, MOG, and VSTM1 was correlated with DNA methylation levels (r2>0.5). Lastly, we identified 4 lncRNAs, 9 miRNAs and 142 mRNAs to construct a lncRNA-miRNA-mRNA ceRNA network. Conclusion: Our results revealed that DNA methylation was altered before and after treatment. Alterations in DNA methylation affected target gene expression and participated in the key biological processes of AML. Therefore, ceRNA networks may provide further insight into the study of favorable therapeutic markers in AML.


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