الفهرس 
Chapter 1 Introduction & Review of LiteratureOnly 14 pages are availabe for public view
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Abstract
Acute Myeloid Leukemia (AML) result from malignant clonal expansion of self-renewing immature myeloid progenitors followed by accumulation of non-functional leukemic blasts in Bone Marrow (BM). AML accounts for high mortality rates and poor outcomes due to high risk of relapse and resistance of relapsed clones to chemotherapy. Researches proposed that relapse in AML is caused by continued survival of a small population of leukemic stem cells (LSCs) after successful complete remission (CR). Researchers had reported that LSCs were determined and discriminated from normal hematopoietic stem cells (nHSCs) using cell membrane surface markers that existed preferentially on LSCs of AML but nHSCs. However, there is a need for new markers to be discovered for better quantification of LSCs. The purpose of this study was to address the prognostic relevance of CD34+/CD38–/TIM3+ LSCs frequency in patients with AML to estimate the prognostic impact of TIM3 expression on AML disease course, the response to chemotherapy and patient outcome. This study was performed on 53 AML patients. Our study concluded that: Identification of LSCs using TIM3 in addition to CD34+/CD38- is better for differentiation between nHSCs and LSCs. Our finding address the LSCs (CD34+/CD38-/TIM3+) percentage cut off (≥0.067%) at AML diagnosis to predict patient response to chemotherapy as well as patient outcome. Quantification of LSCs (CD34+/CD38-/TIM3+) percentage burden at diagnosis could be used as biomarker to refine risk stratification of AML. TIM3 could be considered for targeted therapy in chemo-resistant AML patients.