Vascular endothelial growth factor C—a potent risk factor in childhood acute lymphoblastic leukaemia: an immunocytochemical approach

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To investigate the immunocytochemical expression of vascular endothelial growth factor C (VEGF-C) and its receptors (VEGFR-2 and VEGFR-3) in childhood acute lymphoblastic leukaemia (ALL) blasts and to determine the possible role of this complex in the pathogenesis and prognosis of ALL.

Methods and results

Bone marrow samples were taken from 120 children diagnosed with ALL. An indirect immunocytochemical procedure was performed with the use of monoclonal mouse anti-human antibodies against VEGF-C, VEGFR-2 and VEGFR-3 (diluted 1: 100). The immunocytochemical expression of VEGF-C was confirmed exclusively in the cytoplasm of ALL lymphoblasts (the mean percentage was 36.4 ± 7.2). It was absent from the cytoplasm of normal haematopoietic cells in the control group. No VEGFR-2 or VEGFR-3 expression was detected in the children of either the study or control groups. The risk of induction failure or leukaemic relapse was found to be significant in all VEGF-C+ patients (P < 0.0001 and P < 0.02, respectively; Fisher's exact test).


The absence of VEGF-C in blast cells predicts long-lasting remission in all leukaemic children. Our findings also suggest that leukaemic cell invasion, following VEGF-C-driven lymphangiogenesis, could be related to a mediating role of this peptide produced by blast cells themselves.

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