الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 175 |  |  |
| | | from | 175 | | |
Abstract
Recent studies have provided several insights into understanding acute myeloid leukemia pathogenesis, leukemogenesis, characterization of LSCs and assessment of cell surface markers. Such biological findings have enabled the development of new targeted therapy.
CD200 (an immune checkpoint molecule) is a type-1 transmembrane glycoprotein that belongs to the IgSF and is responsible for inhibitory signaling for immune responses through interaction with its receptor CD200R1. Besides being expressed in the TME, it facilitates tumorigenesis and creates conditions that favor tumor development, growth, and spread. Immune checkpoint molecules regulate immune response pathways to prevent hyperactive immune activity from damaging healthy tissues. In leukemic patients, targeting these key molecules may serve as a valuable therapeutic mechanism to repose immune function and restore the body’s natural defenses against leukemic cells.
CD56 or NCAM-1 is also a cell surface glycoprotein that belongs to the IgSF which plays a great role in formation of the neural circuit, development of the muscles and brain. Being expressed in leukemic cells, it is blamed for metastasis formation (extramedullary leukemia) and tumor progression.
Previous studies have investigated the prognostic significance of CD200 and CD56 in AML, however the results remained controversial. This prompted us to investigate the expression level of CD200 and CD56 in de-novo acute myeloid leukemia patients and to evaluate the prognostic value of their positive expressions.
This study was conducted on 51 newly diagnosed AML patients. All patients were subjected to full history taking, clinical examination, CBC, BM aspiration with examination of Leishman-stained smear, cytochemical analysis, flow-cytometric immunophenotyping of BM blasts using acute leukemia panel and cytogenetic analysis.
A total of 51 newly diagnosed AML patients were tested for CD200 and CD56 expression by flowcytometry at diagnosis.
In the present study, CD200 was found to be highly expressed (74.5%) in AML patients. According to FAB classification in our patients, a significantly higher CD200 expression in M1-M2 subtypes compared to other FAB subtypes (P= 0.006). On the other hand, CD56 was found to be expressed in (9.8%) of AML patients with no significance according to FAB classification in our patients.
In the current study, a statistically significant difference was found between CD200 positive and CD200 negative groups regarding gender (p= 0.045), between CD56 positive and CD56 negative groups regarding age (p= 0.002) but no significance was found between two groups of both markers regarding rest of demographic and clinical data. As regards laboratory parameters, a significant difference was found only between CD56 positive and CD56 negative groups regarding CRP (p= 0.031).
Moreover, this work could not prove any association between either CD200 or CD56 expression and cytogenetic risk stratification of the studied AML patients. Only what we could prove is that CD200 expression is associated with higher incidence of mortality in our study (OR 4.38, p= 0.037) which suggests a negative impact of CD200 expression on survival rate while CD56 is not associated with significant mortality.
In conclusion, in view of the present study, the prognostic value of CD200 and CD56 expression in AML is not clear and remains to be explored. However, CD200 is proved to be associated with higher incidence of mortality in our study. On the other hand, we couldn’t find a significant association between CD56 and mortality. So anti-CD200 and anti-CD56 can be introduced in therapeutic strategies of AML patients for getting promising results.