Table 1.

Patient characteristics at baseline

PV (n = 15)PVR (n = 10)Total (N = 25)
Age in y, median (range) 66 (49-77) 69 (39-78) 66 (39-78) 
Sex, n (%)    
Female 2 (13) 3 (30) 5 (20) 
Male 13 (87) 7 (70) 20 (80) 
ECOG PS    
7 (47) 7 (70) 14 (56) 
8 (53) 3 (30) 11 (44) 
Mutation status, n (%)     
BTK C481 mutant 6 (40) 3 (38) 9 (39) 
BTK C481 wild type 9 (60) 5 (63) 14 (61) 
PLCG2 mutation status, n (%)     
Yes 1 (7) 0 (0) 1 (4) 
No 14 (93) 8 (100) 22 (96) 
del(17p) by FISH, n (%)     
Yes 1 (9) 3 (33) 4 (20) 
No 10 (91) 6 (67) 16 (80) 
TP53 mutation status, n (%)§     
Mutated 3 (20) 3 (38) 6 (26) 
Unmutated 12 (80) 5 (63) 17 (74) 
del(17p) and/or TP53 mutation status, n (%)||     
Yes 3 (27) 4 (50) 7 (37) 
No 8 (73) 4 (50) 12 (63) 
del(11q) by FISH, n (%)     
Yes 4 (36) 4 (44) 8 (40) 
No 7 (63) 5 (56) 12 (60) 
IGHV mutation status, n (%)#     
Mutated 3 (27) 1 (11) 4 (20) 
Unmutated 8 (73) 8 (89) 16 (80) 
Prior lines of systemic therapy, median (range)    
All therapies 1 (1-2) 2 (1-4) 2 (1-4) 
BTKi therapies 1 (0-1) 1 (0-2) 1 (0-2) 
Prior therapies, n (%)    
Anti-CD20 antibody∗∗  11 (73) 7 (70) 18 (72) 
BTKi 11 (73) 6 (60) 17 (68) 
Chemotherapy 8 (53) 6 (60) 14 (56) 
PI3K agent 1 (7) 2 (20) 3 (12) 
Reasons for BTKi discontinuation, n (%)††     
Progressive disease 8 (73) 4 (67) 12 (71) 
Toxicity 3 (27) 2 (33) 5 (29) 
PV (n = 15)PVR (n = 10)Total (N = 25)
Age in y, median (range) 66 (49-77) 69 (39-78) 66 (39-78) 
Sex, n (%)    
Female 2 (13) 3 (30) 5 (20) 
Male 13 (87) 7 (70) 20 (80) 
ECOG PS    
7 (47) 7 (70) 14 (56) 
8 (53) 3 (30) 11 (44) 
Mutation status, n (%)     
BTK C481 mutant 6 (40) 3 (38) 9 (39) 
BTK C481 wild type 9 (60) 5 (63) 14 (61) 
PLCG2 mutation status, n (%)     
Yes 1 (7) 0 (0) 1 (4) 
No 14 (93) 8 (100) 22 (96) 
del(17p) by FISH, n (%)     
Yes 1 (9) 3 (33) 4 (20) 
No 10 (91) 6 (67) 16 (80) 
TP53 mutation status, n (%)§     
Mutated 3 (20) 3 (38) 6 (26) 
Unmutated 12 (80) 5 (63) 17 (74) 
del(17p) and/or TP53 mutation status, n (%)||     
Yes 3 (27) 4 (50) 7 (37) 
No 8 (73) 4 (50) 12 (63) 
del(11q) by FISH, n (%)     
Yes 4 (36) 4 (44) 8 (40) 
No 7 (63) 5 (56) 12 (60) 
IGHV mutation status, n (%)#     
Mutated 3 (27) 1 (11) 4 (20) 
Unmutated 8 (73) 8 (89) 16 (80) 
Prior lines of systemic therapy, median (range)    
All therapies 1 (1-2) 2 (1-4) 2 (1-4) 
BTKi therapies 1 (0-1) 1 (0-2) 1 (0-2) 
Prior therapies, n (%)    
Anti-CD20 antibody∗∗  11 (73) 7 (70) 18 (72) 
BTKi 11 (73) 6 (60) 17 (68) 
Chemotherapy 8 (53) 6 (60) 14 (56) 
PI3K agent 1 (7) 2 (20) 3 (12) 
Reasons for BTKi discontinuation, n (%)††     
Progressive disease 8 (73) 4 (67) 12 (71) 
Toxicity 3 (27) 2 (33) 5 (29) 

Total percentage might be different than the sum of the individual components because of rounding. Molecular features were analyzed by a central research laboratory. Percentages were calculated for patients with available data.

BTKi, Bruton tyrosine kinase inhibitor; ECOG PS, Eastern Cooperative Oncology Group Performance Status; FISH, fluorescence in situ hybridization; IGHV, immunoglobulin heavy variable; PI3K, phosphatidylinositol 3-kinase.

2 patients had missing data (PV: 0; PVR: 2).

2 patients had missing data (PV: 0; PVR: 2).

5 patients had missing data (PV: 4; PVR: 1).

§

2 patients had missing data (PV: 0; PVR: 2).

6 patients had missing data (PV: 4; PVR: 2).

5 patients had missing data (PV: 4; PVR: 1).

#

5 patients had missing data (PV: 4; PVR: 1).

∗∗

Includes both patients who had anti-CD20 as monotherapy and as combination therapy.

††

Calculated as the percentage of patients who received prior BTK inhibitor. If >1 reason was noted for discontinuation, disease progression took priority.

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