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Original Article

High expression of CD7 on CD34+ cells is not linked to deletion of derivative chromosome 9 or lack of dendritic cells in chronic myeloid leukaemia

, , , &
Pages 93-98 | Received 05 May 2007, Accepted 27 Jun 2007, Published online: 08 Jul 2009
 

Abstract

Objective. High expression of CD7 on CD34+ cells (>20 %) has been shown to be associated with inferior prognosis in chronic myeloid leukaemia (CML), but the reason has not been unravelled. We set out to investigate whether lack of dendritic cells or der(9)t(9;22)(q34;q11) deletions might be correlated with increased CD7 expression on CD34+ cells in CML. Material and methods. We identified 43 patients in our cohort of CML patients in the first chronic phase in whom we were able to assess the expression of CD7 on CD34+ cells. der(9)t(9;22) deletions were evaluated by FISH (fluorescent in situ hybridization) analyses and the proportions of plasmacytoid and myeloid dendritic cells were assessed by flow cytometry. Results. High and low expressions of CD7 on CD34+ cells were found in 19 and 24 patients, respectively. Two out of 20 patients examined had a der(9)t(9;22)(q34;11) deletion, one patient with high expression and one with low expression of CD7 on CD34+ cells. The proportions of plasmacytoid dendritic cells (PDCs) and myeloid dendritic cells (MDCs) were reduced in a majority of patients in our cohort, but no correlation was found between high or low expression of CD7 on CD34+ cells and the proportion of dendritic cells. Conclusions. A high proportion of CD34+CD7+ cells in patients with CML is not associated with der(9)t(9;22)(q34;q11) deletions. Nor did we find any correlation between CD7 expression on CD34+ cells and lack of dendritic cells. High expressions of CD7 on CD34+ cells and der(9)t(9;22)(q34;q11) deletions seem to be independent prognostic markers in CML.

Acknowledgements

Y.F., A.P.N. and G.E.T. designed the study and wrote the manuscript. Y.F. and A.P.N. procured the patient samples and performed the flow cytometric and statistical analyses. Y.F. and A.P.N. contributed equally to this project. S.H. was responsible for the FISH‐analyses. F.L.J. supervised the flow cytometric analyses. S.H. and F.L.J. critically revised the manuscript and approved the final revision. The authors declare that they have no potential conflict of interests.

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