Table 1.

Growth inhibition and apoptosis due to rituximab alone

Cell lineGrowth inhibition, %PRituximab, % annexin V+ cellsRituximab-induced sub-G1DNA
DHL-4 54 < .0001 23 Weak 
Daudi 24 .025 13 Weak 
FL-18 17 NS 12 No  
Granta 519 20 .005 No  
NCEB-1 30 .002 No 
OCI Ly8 42 .003 No 
Raji 13 NS 12 No 
Ramos 18 .002 No 
Tab 83 .0001 17 Weak 
Cell lineGrowth inhibition, %PRituximab, % annexin V+ cellsRituximab-induced sub-G1DNA
DHL-4 54 < .0001 23 Weak 
Daudi 24 .025 13 Weak 
FL-18 17 NS 12 No  
Granta 519 20 .005 No  
NCEB-1 30 .002 No 
OCI Ly8 42 .003 No 
Raji 13 NS 12 No 
Ramos 18 .002 No 
Tab 83 .0001 17 Weak 

Columns 1 and 2 demonstrate the percentage of growth inhibition induced by saturating doses of rituximab (10 μg/mL) and the corresponding P values, derived from 3 or more separate experiments. Growth inhibition was calculated as 1 − experimental CPM divided by control CPM, and growth inhibition was reported as a percentage with the highest (least significant) Pvalue. Two cell lines, FL-18 and Raji, had insignificant growth inhibition, whereas in all other cell lines, growth inhibition was highly statistically significant. Column 3 summarizes the mean percentage of cells (taken from at least 3 experiments) that become annexin V+ (minus control) following treatment with 48 hours of rituximab (10 μg/mL). Results range from 5% to 23% of cells. Column 4 summarizes the effects of rituximab alone on DNA fragmentation. Three cell lines, following exposure to rituximab (10 μg/mL) for 72 hours, have weak, but reproducible and statistically significant, increases in sub-G1 DNA content.

NS indicates not significant.

Close Modal

or Create an Account

Close Modal
Close Modal