الفهرس 
Chronic lymphocytic leukemiaOnly 14 pages are availabe for public view
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Abstract
Of all leukemias, chronic lymphocytic leukemia shows the highest variability in its clinical presentation and course. CLL can present as an aggressive and life threating leukemia or as an indolent form that will not require treatment over decades. The currently available clinical staging systems for CLL are simple and inexpensive but lack accuracy to predict disease progression and survival on an individual basis. The increased understanding of the key events of molecular pathogenesis has provided a plethora of novel molecular and biological factors that correlate with the outcome of CLL.
The median age for CLL diagnosis is between 67 years and 72 years and more males are affected than females (ratio of 1.7:1). However, there is an increase in the proportion of younger patients diagnosed with early stage CLL and minimal symptoms due to more frequent blood testing.
CLL is characterized by the clonal proliferation and accumulation of mature CD5+ B cells within the blood, bone marrow, lymph nodes and spleen. It is now well recognized that central to that are several genetic and molecular events that are responsible for development of CLL. The diagnosis of CLL is established by blood count, blood smear and immunophenotyping of the circulating lymphocytes.
CD73 is a cell membrane anchored surface enzyme that catalyzes the extracellular conversion of AMP to adenosine, which controls many physiological and pathophysiological events including fine tuning of the immune system. This process represents the last step in the extracellular adenine nucleotide breakdown after CD39 dependent conversion of ATP to ADP and AMP. Numerous studies have investigated the role of CD73 in different types of cancers.
This study aimed to evaluate CD73 expression in peripheral blood in CLL patients and to correlate them to different disease characteristics. The study included 40 subjects. Twenty five CLL patients in whom diagnosis was confirmed by immunophenotyping on peripheral blood. The study also included fifteen age and sex matched normal controls.
All patients were subjected to the followings: Full history taking and clinical examination, chest, abdominal and pelvic C.T scan and laboratory investigations which include CBC and blood film, LDH and β2 microglobulin levels and routine immunophenotyping. In addition to, both patients and controls had CD19, CD38 and quantitative analysis of CD73 by immunophenotyping.
This study has shown that CD73 expression was significantly lower on clonal B lymphocytes and on T lymphocytes in patients with CLL compared with controls (p value <0.001). However, there was no significant difference in CD38 expression by the two groups (p value >0.05).
In addition, No significant correlation between CD73 expression and clinical stage of the disease was found except for CD73 expression on T lymphocytes. It was significantly lower in stage C compared to stage A and B of the disease (p value 0.05).
In our study, there was no correlation between CD73 expression and the response to therapy, however the number evaluable for response was small and follow up was short. Our study and others have shown low CD73 expression in CLL patients compared to normal control and this might have a role in tumorgenesis in CLL due to lack of the suppressive effect of adenosine on the immune system with consequent inappropriate stimulation , immortalisation and/or clonal expansion of B-cells.
It is recommended to do a quantitative CD73 analysis on large number of CLL patients and on other B-lymphoproliferative disorders to examine the possibility of adding it to CLL scoring system.