Research Papers:
Clinical impact of CD200 expression in patients with acute myeloid leukemia and correlation with other molecular prognostic factors
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Abstract
Daniela Damiani1, Mario Tiribelli1, Donatella Raspadori2, Santina Sirianni2, Alessia Meneghel1, Margherita Cavalllin1, Angela Michelutti1, Eleonora Toffoletti1, Antonella Geromin1, Erica Simeone1, Monica Bocchia2, Renato Fanin1
1Division of Hematology and Bone Marrow Transplantation, Azienda Ospedaliero-Universitaria di Udine, Udine, Italy
2Division of Hematology, University of Siena, Siena, Italy
Correspondence to:
Daniela Damiani, e-mail: [email protected]
Keywords: CD200, acute myeloid leukemia, prognosis, survival
Received: May 18, 2015 Accepted: August 07, 2015 Published: August 18, 2015
ABSTRACT
CD200, a protein belonging to the immunoglobulin superfamily, has been associated with a poor prognosis in lymphoproliferative disorders and in acute leukemia. We studied the expression of CD200 in a series of 244 patients with diagnosis of acute myeloid leukemia (AML), to evaluate its impact on outcome and its possible association with other known prognostic factors.
CD200 was found in 136/244 (56%) patients, in 41 of whom (30%) with high intensity of expression (MFI ≥ 11). CD200 was more frequent in secondary compared to de novo leukemia (p = 0.0006), in CD34 positive cases (p = 0.00001), in Bcl2 overexpressing cases (p = 0.01), in those wild-type Flt3 (p = 0.004) and with favorable or unfavorable compared to intermediate karyotype (p = 0.0003). CD200+ patients have a two-fold lower probability to attain complete remission, both in univariate (p = 0.006) and multivariate (p = 0.04) analysis. The negative impact of CD200 was found also in overall survival (p = 0.02) and was correlated with the intensity of expression of the molecule (p = 0.024). CD200 has an additive negative impact on survival in patients with unfavorable cytogenetic (p = 0.046) and in secondary leukemia (p = 0.05), and is associate with a worsening of outcome in patients with favorable biological markers, such as mutated NPM (p = 0.02), wild-type Flt3 (p = 0.034), negativity of CD34 (p = 0.03) and of CD56 (p = 0.03).
In conclusion, CD200 is emerging as both a prognostic factor and a potential target of novel therapeutic approaches for AML, aiming to reverse the “do not eat me” signal of CD200 or to manipulate the suppressive immune microenvironment induced by CD200 binding to its receptor.
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