CD31 density is a novel risk factor for patients with B-cell chronic lymphocytic leukaemia.
CD31 is the physiological ligand for CD38. CD38 expression in a high percentage of malignant cells is a risk factor for patients with B-cell chronic lymphocytic leukaemia (B-CLL). A previous investigation demonstrated that quantification of CD38 improves upon the prognostic value of the percentage expression. A recent study states that the percentage of CD31 expression is not predictive in B-CLL. We reassessed the predictive power of CD31 in a cohort of 120 patients with B-CLL. Peripheral blood cells were stained with PCP-labelled anti (alpha)-CD19, FITC-alpha-CD5 and PE-alpha-CD31 antibodies. CD31 expression was quantified using beads of specific antibody binding capacity and the density was correlated with clinical outcome. End points were disease-specific survival and time to treatment (TTT). We report that CD31 density was significantly lower in the group of patients with Binet stage B and C of disease progression (P=0.0003). There was an inverse, significant correlation between CD31 and CD38 densities (R= -0.281, P=0.002). All CLL-related deaths occurred in patients with low CD31 density. Low CD31 predicted for poor disease outcome (survival, P=0.0087; TTT, P=0.0064) and identified Binet stage A patients (survival, P=0.0350; TTT, P=0.0716) and those with low CD38 (survival: all patients, P<0.0001; stage A, P=0.003) who followed a more aggressive clinical course. Disease-specific survival of patients with low CD31 and high CD38 densities was significantly shorter than all other groups. In addition, low CD31 density was a poor risk factor irrespective of patient age (survival: all patients, P=0.045; stage A, P=0.021) and identified patients with Binet stage B/C as the highest risk group (P<0.0001). In conclusion, low CD31 density is an adverse prognostic indicator in B-CLL. Also, low CD31 density enhances the prognostic power of CD38 density. The interaction between CD31 and CD38 and its clinical significance in B-CLL requires further investigation.
Mainou-Fowler
Tryfonia
T
Academic Haematology, School of Clinical and Laboratory Sciences, William Leech Building, The Medical School, Framlington Place, Newcastle upon Tyne, Tyne and Wear, NE2 4HH, UK. tryfonia.mainou-fowler@ncl.ac.uk
Porteous
Alistair
A
Nicolle
Annette
A
Proctor
Stephen John
SJ
Anderson
John James
JJ
Summerfield
Geoffrey
G
D051997:ADP-ribosyl Cyclase 1 / Q000032:analysis; D000368:Aged; D000369:Aged, 80 and over; D005260:Female; D006801:Humans; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000209:etiology* / Q000276:immunology / Q000401:mortality; D008297:Male; D008875:Middle Aged; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis*; D012307:Risk Factors
D019408:Platelet Endothelial Cell Adhesion Molecule-1; D051997:ADP-ribosyl Cyclase 1