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Adenosine Deaminase 1 as a Biomarker for Diagnosis and Monitoring of Patients with Acute Lymphoblastic Leukemia

. Pui CH, Relling MV, Downing JR. Acute lymphoblastic leukemia. The New England Journal of Medicine 2004; 350: 1535–48. 5. Pui CH, Robison LL, Look AT. Acute lymphoblastic leukaemia. Lancet 2008; 371: 1030–43. 6. Collinson P. Laboratory Medicine is faced with the evolution of medical practice. J Med Biochem 2017; 36: 211–5. 7. Skarar DN, Hossain I, Shoab AKM, Amin R. Adenosine Deaminase (ADA) in Tuberculous Meningitis. Bangladesh J Medicine 2014; 25: 61–71. 8. Mishra SK, Sah JP, Awasthi G, Sharma R. Adenosine Deaminase activity in Plasma of

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Variants in TPMT, ITPA, ABCC4 And ABCB1 Genes as Predictors of 6-Mercaptopurine Induced Toxicity in Children with Acute Lymphoblastic Leukemia

References 1. Pui C, Mullighan CG, Evans WE, Relling MV. Pediatric acute lymphoblastic leukemia: where are we going and how do we get there? Blood 2012; 120(6): 1-3. 2. Kim H, Kang HJ, Kim HJ, Jang MK, Kim NH, Oh Y, et al. Pharmacogenetic Analysis of Pediatric Patients with Acute Lymphoblastic Leukemia: A Possible Association between Survival Rate and ITPA Polymorphism. PLoS One 2012; 7(9): 1-10. 3. Paugh SW, Stocco G, Evans WE. Pharmacogenomics in pediatric leukemia. Curr Opin Pediatr 2010; 22: 703

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Application of targeted next generation sequencing for the mutational profiling of patients with acute lymphoblastic leukemia

missense mutations. References 1 Pui CH, Robison LL, Look AT. Acute lymphoblastic leukaemia. Lancet 2008; 371: 1030–43. 10.1016/S0140-6736(08)60457-2 Pui CH Robison LL Look AT Acute lymphoblastic leukaemia Lancet 2008 371 1030 – 43 2 Mrozek K, Harper DP, Aplan PD. Cytogenetics and molecular genetics of acute lymphoblastic leukemia. Hematol Oncol Clin North Am 2009; 23: 991–1010. 10.1016/j.hoc.2009.07.001 Mrozek K Harper DP Aplan PD Cytogenetics and molecular genetics of acute lymphoblastic leukemia Hematol Oncol Clin North

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The use of biomarkers in detecting subclinical cardiotoxicity in doxorubicin-based treatment for paediatric patients with acute lymphoblastic leukaemia

Abstract

The international standard protocol for acute lymphoblastic leukaemia (ALL), the most common haemato-oncological pathology at paediatric age, uses anthracyclines as antitumor agents, potentially associated with early or late onset cardiac damage. Currently, echocardiography is the gold standard in the diagnosis of cardiotoxicity, but several biomarkers are evaluated as a possible replacement, pending more extensive clinical studies. We started a prospective study in order to determine the role of two biomarkers, troponin and heart-type fatty acid binding protein, in the evaluation of cardiotoxicity in children over one year of age, diagnosed with ALL. Between February 2015 and April 2016, 20 patients were enrolled and monitored at diagnosis, during chemotherapy and four months after the end of reinduction, through cardiac evaluation and dosing of those two markers in five different points of the treatment protocol. During the first year of follow-up, the patients did not develop clinical signs of cardiac damage, but the study showed a slight increase in troponin levels during chemotherapy, with the return to baseline value after treatment cessation, and also a correlation with the total dose of anthracyclines given to the patient. On the other hand, the second biomarker, heart-type fatty acid binding protein, did not seem to be useful in detecting subclinical cardiac damage in these patients.

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The impact of immunological and biomolecular investigations on the outcome of children with acute lymphoblastic leukemia - experience of IIIrd Paediatric Clinic Timisoara

References 1. Inaba H, Greaves M, Mullighan CG. Acute lymphoblastic leukaemia. The Lancet. 2013 Jun;381(9881):1943-55. DOI: 10.1016/S0140-6736(12)62187-4 2. Bartram CR, Schrauder A, Köhler R, Schrappe M. Acute lymphoblastic leukemia in children: treatment planning via minimal residual disease assessment. Dtsch Arzteblatt Int. 2012 Oct;109(40):652-8. 3. Harrison CJ. Cytogenetics of paediatric and adolescent acute lymphoblastic leukaemia. Br J Haematol. 2009 Jan;144(2):147-56. DOI: 10.1111/j.1365-2141.2008.07417.x

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Expression pattern of long non-coding RNA growth arrest-specific 5 in the remission induction therapy in childhood acute lymphoblastic leukemia

Introduction Among pediatric malignancies, acute lymphoblastic leukemia (ALL) is the most common hematological and overall malignancy, contributing to 30% of diagnosed cancers and around 80% of all pediatric leukemias. Pediatric ALL is a malignancy with one of the highest cure rates, achieved by treating the patients with the internationally recognised treatment protocols like the Berlin-Frankfurt-Munster (BFM) protocol ( 1 , 2 , 3 ). Risk stratification of ALL is para mount in choosing the effective treatment strategy. Hence, risk stratification is already

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Mathematical model to predict methotrexate elimination in children with acute lymphoblastic leukemia

. Long-term results of NOPHO ALL-92 and ALL-2000 studies of childhood acute lymphoblastic leukemia. Leukemia. 2010;24(2):345-54. DOI: 10.1038/leu.2009.251 12. Mitchell C, Richards S, Harrison CJ, Eden T. Long-term follow-up of the United Kingdom medical research council protocols for childhood acute lymphoblastic leukaemia, 1980-2001. Leukemia. 2010;24(2):406-18. DOI: 10.1038/leu.2009.256 13. Evans WE, Relling MV, Rodman JH, Crom WR, Boyett JM, Pui CH. Conventional compared with individualized chemotherapy for childhood acute

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Selected Aspects of Angiogensis in Haematological Malignancies

and myelodysplastic syndromes. Blood 2000; 96(6): 2240-2245. [4] AVRAMIS IA, PANOSYAN EH, DOREY F, HOLCENBERG JS, AVRAMIS VI. Children's Oncology Group., Correlation between high vascular endothelial growth factor-A serum levels and treatment outcome in patients with standard-risk acute lymphoblastic leukemia: a report from Children's Oncology Group Study CCG-1962. Clin Cancer Res 2006; 12(23): 6978-6984. [5] BACHELDER RE, CRAGO A, CHUNG J, WENDT MA, SHAW LM, ROBINSON G, MERCURIO AM. Vascular endothelial growth factor is an autocrine

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Infant acute leukemia with lineage switch at relapse expressing a novel t(4;11)(q21;q23) MLL-AF4 fusion transcript

References 1. De Braekeleer E, Douet-Guilbert N, Le Bris MJ, Basinko A, Morel F, De Braekeleer M. Gene expression profiling of adult t(4;11)(q21;q23)-associated acute lymphoblastic leukemia reveals a different signature from pediatric cases. Anticancer Res. 2012 Sep;32(9):3893-9 2. De Braekeleer M, Morel F, Le Bris MJ, Herry A, Douet-Guilbert N. The MLL gene and translocations involving chromosomal band 11q23 in acute leukemia. Anticancer Res. 2005 May-Jun;25(3B):1931-44 3. Drexler HG, Quentmeier H

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Methotrexate-Associated Biochemical Alterations in a Patient with Chronic Neurotoxicity

References Walker RW, Allen JC, Rosen G, Caparros B. Transient cerebral dysfunction secondary to high-dose methotrexate. J Clin Oncol 1986; 4: 1845-50. García-Tena J, López-Andreu JA, Ferrís J, Menor F, Mulas F, Millet E, et al. Intrathecal chemotherapy-related myeloencephalopathy in a young child with acute lymphoblastic leukemia. Pediatr Hematol Oncol 1995; 12: 377-85. Oka M, Terae S, Kobayashi R, Sawamura Y, Kudoh K, Tha KK, et al. MRI in methotrexate

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