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Acute Lymphocytic Leukemia (ALL) Assignment

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Added on  2020-04-21

Acute Lymphocytic Leukemia (ALL) Assignment

   Added on 2020-04-21

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Running head: ACUTE LYMPHOCYTIC LEUKEMIA 1Annotated bibliography on Acute Lymphocytic Leukemia (ALL)Frederick WilsonColumbia Southern University
Acute Lymphocytic Leukemia (ALL) Assignment_1
ACUTE LYMPHOCYTIC LEUKEMIA2Akin, D. F., Oner, D. A., Sipahi, K., Mumcuoglu, M., Kurekci, E., Ezer, U., & Akar, N. (2017).Screening of polymorphisms in the folate pathway in Turkish pediatric AcuteLymphoblastic Leukemia patients.Egyptian Journal of Medical Human Genetics, 18(4),p349-353. 5p.The authors investigated polymorphisms of folate related genes that increase thesusceptibility to childhood ALL. Genotyping, RFLP AND RT-PCT screened 5polymorphisms. The article was chosen as it showed an association between TYMS1494del6 and ALL and demonstrated lack of association with DHFR, MTHFR and CBSgenes.Davila, M. L., Riviere, I., Wang, X., Bartido, S., Park, J., Curran, K., ... & Qu, J. (2014).Efficacy and toxicity management of 19-28z CAR T cell therapy in B cell acutelymphoblastic leukemia.Science translational medicine,6(224), 224ra25-224ra25.The authors aimed to assess the effectiveness of autologous T cells that expressed 19-28zchimeric antigen receptor on ALL. It identified the diagnostic criteria for severe cytokinerelease syndrome and found serum C-reactive proteins to be reliable indicators. Thisarticle was chosen as it provided strong evidence for conduction of T-cell therapy.Inaba, H., Greaves, M., & Mullighan, C. G. (2013). Acute lymphoblastic leukaemia.TheLancet,381(9881), 1943-1955.This article helped in the identification of the multifactorial causation, geneticsusceptibility and exposure rates that increase the likelihood of a person becomingaffected with ALL. The study was chosen as it identified novel structural mutations andgenetic changes through genome wide profiling and also helped in defining new diseasesubtypes and treatment response.
Acute Lymphocytic Leukemia (ALL) Assignment_2

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