الفهرس 
Acute Myeloid LeukemiaOnly 14 pages are availabe for public view
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Abstract
Acute myeloid leukemia (AML) is characterized by abnormal proliferation of undifferentiated and non-functional hematopoietic cells (Leukemic blasts) in the bone marrow.
Diagnosis and sub-classification by FAB and WHO criteria require combination of morphology, cytochemistry, cytogenetics and immunophenotyping with flowcytometry, genetic, biological and clinical features to define specific disease entities.
AML still has a dismal outcome. The poor survival is mainly associated with chemotherapy resistance and AML relapse. Previous reports have shown that AML relapse and chemotherapeutic drug resistance result from a small population of leukemia-initiating cells or leukemic stem cells (LSCs). AML-LSCs are enriched in the CD34+/CD38- population. LSCs also express certain unique cell surface markers such as CD123, CD117, CD90, CD47 and CD96.
CD96 (TACTILE) is a transmembrane glycoprotein, which is expressed by T and NK cells but not on majority of B cells, monocytes and granulocytes in human peripheral blood cells.
Recent studies suggested that CD96 was a putative marker expressed by LSCs in AML patients. However, few studies were conducted to investigate its role as a prognostic marker and its relation to response to induction chemotherapy.
This study included 40 newly diagnosed adult de novo AML patients (before initiation of therapy) and 10 non-leukemic adult subjects as controls. CD96 expression was evaluated among CD34+/CD38- cell population using flowcytometry.
In this study, the expression of CD96 is observed in 60% of AML cases and this expression was significantly higher in AML patients than controls.
Only a significant relation was found between CD96 expression and fever, while no significant association between CD96 expression and other clinical parameters.
The study showed no statistically significant relation with the standard prognostic factors, but there was a statistically highly significant correlation between CD96 expression and response to induction chemotherapy was found.
In conclusion, our study identified CD96 as a promising marker for LSCs in AML patients. Its frequent expression in the CD34+/CD38- LSC population and association with lower response rate to induction chemotherapy suggest its potential as a valuable tool for LSC identification, targeted therapy development and improved treatment outcome prediction in AML.