Treatment history
. | DR (n = 30) . | DE (n = 65) . | P value∗ . |
---|---|---|---|
Number of lines of therapy, median (range) | |||
Total | 6 (3-11) | 3 (1-8) | <.05 |
Before the landmark time point | 4 (1-8) | 3 (0-7) | .01 |
After the landmark time point | 2 (0-5) | 0 (0-4) | <.05 |
Refractoriness, n (%) | |||
cBTKi | 29 (96.7) | 19 (29.2) | <.001 |
BCL2i | 30 (100.0) | 8 (12.3) | <.001 |
ncBTKi | 11 (36.7) | 3 (4.6) | <.001 |
PI3Ki | 9 (30.0) | 2 (3.1) | <.001 |
3R to cBTKi, BCL2i, and ncBTKi | 10 (33.3) | 0 (0.0) | <.001 |
3R to cBTKi, BCL2i, and PI3Ki | 8 (26.7) | 0 (0.0) | <.001 |
4R to cBTKi, BCL2i, ncBTKi, and PI3Ki | 5 (16.7) | 0 (0.0) | .002 |
Types of therapy at any time point, n (%) | |||
cBTKi ± CD20 mAb | 30 (100.0) | 65 (100.0) | NS |
BCL2i ± CD20 mAb | 30 (100.0) | 65 (100.0) | NS |
CIT | 25 (83.3) | 42 (64.6) | NS (.06) |
PI3Ki ± CD20 mAb | 11 (36.7) | 18 (27.7) | NS |
ncBTKi | 13 (43.3) | 8 (12.3) | <.001 |
Concurrent cBTKi/BCL2i ± CD20 mAb | 10 (33.3) | 10 (15.4) | .046 |
allo SCT | 5 (16.7) | 7 (10.8) | NS |
CAR T | 8 (26.7) | 2 (3.1) | .001 |
Bispecific antibody (CD3 × CD20) | 1 (3.3) | 2 (3.1) | NS |
BTK degrader | 2 (6.7) | 0 (0.0) | NS |
Types of therapy after the landmark time point, n (%)† | |||
ncBTKi | 10 (34.5) | 2 (11.8) | NS |
Concurrent cBTKi/BCL2i | 8 (27.6) | 2 (11.8) | NS |
CAR T | 7 (24.1) | 2 (11.8) | NS |
CIT | 5 (17.2) | 3 (17.6) | NS |
cBTKi ± CD20 mAb | 5 (17.2) | 3 (17.6) | NS |
allo SCT | 3 (10.3) | 5 (29.4) | NS |
PI3Ki ± CD20 mAb | 6 (20.7) | 0 (0.0) | NS (.07) |
BCL2i + CIT | 3 (10.3) | 2 (11.8) | NS |
Bispecific antibody (CD3xCD20) | 1 (3.4) | 2 (11.8) | NS |
BTK degrader | 2 (6.9) | 0 (0.0) | NS |
BCL2i ± CD20 mAb | 0 (0.0) | 1 (5.9) | NS |
BCL2i + PI3Ki | 0 (0.0) | 1 (5.9) | NS |
. | DR (n = 30) . | DE (n = 65) . | P value∗ . |
---|---|---|---|
Number of lines of therapy, median (range) | |||
Total | 6 (3-11) | 3 (1-8) | <.05 |
Before the landmark time point | 4 (1-8) | 3 (0-7) | .01 |
After the landmark time point | 2 (0-5) | 0 (0-4) | <.05 |
Refractoriness, n (%) | |||
cBTKi | 29 (96.7) | 19 (29.2) | <.001 |
BCL2i | 30 (100.0) | 8 (12.3) | <.001 |
ncBTKi | 11 (36.7) | 3 (4.6) | <.001 |
PI3Ki | 9 (30.0) | 2 (3.1) | <.001 |
3R to cBTKi, BCL2i, and ncBTKi | 10 (33.3) | 0 (0.0) | <.001 |
3R to cBTKi, BCL2i, and PI3Ki | 8 (26.7) | 0 (0.0) | <.001 |
4R to cBTKi, BCL2i, ncBTKi, and PI3Ki | 5 (16.7) | 0 (0.0) | .002 |
Types of therapy at any time point, n (%) | |||
cBTKi ± CD20 mAb | 30 (100.0) | 65 (100.0) | NS |
BCL2i ± CD20 mAb | 30 (100.0) | 65 (100.0) | NS |
CIT | 25 (83.3) | 42 (64.6) | NS (.06) |
PI3Ki ± CD20 mAb | 11 (36.7) | 18 (27.7) | NS |
ncBTKi | 13 (43.3) | 8 (12.3) | <.001 |
Concurrent cBTKi/BCL2i ± CD20 mAb | 10 (33.3) | 10 (15.4) | .046 |
allo SCT | 5 (16.7) | 7 (10.8) | NS |
CAR T | 8 (26.7) | 2 (3.1) | .001 |
Bispecific antibody (CD3 × CD20) | 1 (3.3) | 2 (3.1) | NS |
BTK degrader | 2 (6.7) | 0 (0.0) | NS |
Types of therapy after the landmark time point, n (%)† | |||
ncBTKi | 10 (34.5) | 2 (11.8) | NS |
Concurrent cBTKi/BCL2i | 8 (27.6) | 2 (11.8) | NS |
CAR T | 7 (24.1) | 2 (11.8) | NS |
CIT | 5 (17.2) | 3 (17.6) | NS |
cBTKi ± CD20 mAb | 5 (17.2) | 3 (17.6) | NS |
allo SCT | 3 (10.3) | 5 (29.4) | NS |
PI3Ki ± CD20 mAb | 6 (20.7) | 0 (0.0) | NS (.07) |
BCL2i + CIT | 3 (10.3) | 2 (11.8) | NS |
Bispecific antibody (CD3xCD20) | 1 (3.4) | 2 (11.8) | NS |
BTK degrader | 2 (6.9) | 0 (0.0) | NS |
BCL2i ± CD20 mAb | 0 (0.0) | 1 (5.9) | NS |
BCL2i + PI3Ki | 0 (0.0) | 1 (5.9) | NS |
3R, triple refractory; 4R, quadruple refractory; CD20 mAb, anti-CD20 monoclonal antibody; NS, not significant; PI3Ki, phosphoinositide 3-kinase inhibitor.
Wilcoxon rank-sum test, Pearson χ2 test, and Fisher exact test were used to compare continuous and categorical variables between DR and DE patients. P values were shown for statistically significant comparisons (bold) or those close to .05.
Percentage of patients who received treatment after the landmark time point (29 DR and 17 DE patients).