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Transformation of Aggressive Non-Hodgkin Lymphoma in Acute Lymphoblastic Leukemia

-cell Lymphoma. Leg Type. Acta Derm Venereol . 2016;96:245-250. 8. Pui CH, Evans WE. Treatment of Acute Lymphoblastic Leukemia. N Engl J Med . 2006;354:166-178.

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Association between SLC19A1 gene polymorphism and high dose methotrexate toxicity in childhood acute lymphoblastic leukaemia and non Hodgkin malignant lymphoma: introducing a haplotype based approach

Tanigawara Y Influence of MTHFR and RFC1 polymorphisms on toxicities during maintenance chemotherapy for childhood acute lymphoblastic leukemia or lymphoma J Pediatr Hematol Oncol 2008 30 347 52 10.1097/MPH.0b013e318165b25d 15 Faganel Kotnik B, Grabnar I, Bohanec Grabar P, Dolžan V, Jazbec J. Association of genetic polymorphism in the folate metabolic pathway with methotrexate pharmacokinetics and toxicity in childhood acute lymphoblastic leukaemia and malignant lymphoma. Eur J Clin Pharmacol 2011; 67 : 993-1006. 10.1007/s00228-011-1046-z Faganel Kotnik

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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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Original Research. The Evaluation of Caries Severity Index and Dental Hypoplasia in Children with Acute Lymphoblastic Leukemia. Results from a Romanian Medical Center

References 1. Kaste SC, Goodman P, Leisenring W. Impact of Radiation and Chemotherapy on Risk of Dental Abnormalities: A Report from the Childhood Cancer Survivor Study. Cancer. 2009;115:5817-5827. 2. Welbury RR, Craft AW, Murray JJ, Kernahan J. Dental health of survivors of malignant disease. Arch Dis Child. 1984;59:1186-1187. 3. Kaste SC, Hopkins KP, Jones D, Crorn D, Greenwald CA, Santana VW. Dental abnormalities in children treated for acute lymphoblastic leukemia. Leukemia. 1997

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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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Gingival health in children in the different phases of acute lymphoblastic leukemia

analysis and periodontal status in children with atopy. I nterv Med Appl Sci. 2017;9(4):199-203. 5. Arigbede AO, Babatope BO, Bamidele MK: Periodontitis and systemic diseases: A literature review. J Indian Soc Periodontol. 2012;16(4):487-91. 6. Hunger SP, Lu X, Devidas M, Camitta BM, Gaynon PS, Winick NJ et al. Improved survival for children and adolescents with acute lymphoblastic leukemia between 1990 and 2005: a report from the children’s oncology group. J Clin Oncol. 2012;30(14):1663-69. 7. Lauritano D, Petruzzi M, Fumagalli T, Giacomello MS

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Acute Lymphoblastic Leukemia after previously treated, relapsed Chronic Lymphocytic Leukemia: A Case Report

Abstract

We present the case of a 71-year-old woman diagnosed with chronic lymphocytic leukemia who received multiple chemotherapeutic lines and evolved to acute lymphoblastic leukemia. The patient was Rai stage 0 at the time of the diagnosis and was monitored for almost 9 years. After that, the disease progressed and the patient began chemotherapy (fludarabine/cyclophosphamide combination), obtained complete remission and relapsed one year later after finishing treatment. She received multiple therapeutic regimens, accompanied by multiple infectious complications. After 8 years of evolution since she started chemotherapy, bone marrow aspirate and immunophenotyping revealed acute lymphoblastic leukemia. The occurrence of acute leukemia in CLL is rare and may arise from the same clone; however, most cases appear after patients have received chemotherapy, suggesting that they are therapy-related.

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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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Quercetin, Menadione, Doxorubicin combination as a potential alternative to Doxorubicin monotherapy of acute lymphoblastic leukemia

Abstract

Doxorubicin is a widely used chemotherapeutic drug, effective on patients with acute lymphoblastic leukemia but associated with significant long term cardio-toxicity. Menadione (vitamine K3) and the flavonoid quercetin are known as strong apoptogens in human leukemia Jurkat T cells.

We explored the potential synergic cytotoxic effects of doxorubicin in association with quercetin and Menadione in this cellular model for acute lymphoblastic leukemia.

Cellular viability, apoptosis, necrosis oxidative stress and cellular cycle were determined by flow cytometry utilizing Jurkat lymphoblasts labeled with Annexin V-FITC/7-AAD, CM-H2DCFDA/7-AAD and propidium iodide respectively.

Results indicate a dose-dependent oxidative-stress generation, cell cycle arrest and apoptosis induction by doxorubicin alone, correlated with a decrease of the required doses when the anticancer drug was associated with quercetin and menadione, hence supporting the theory of an additive cytotoxic effect on leukemia cells.

Introducing QC-MD combinations in leukemia doxorubicin-based treatment could significantly increase the treatment’s efficacy. The main mechanism responsible for this effect appears to be the increase in DOX affinity for DNA, which enables lowering of the therapeutic dose.

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