Table 1 Patient demographics and clinical characteristics at baseline and BOR per INV for all treated, WES-evaluable, RNA-seq–evaluable and CD3 IHC-evaluable patients

From: Inflammation and mutational burden differentially associated with nivolumab or ipilimumab combination efficacy in colorectal cancer

 

All treated (n = 193)

WES-evaluable (n = 59)

RNA-seq–evaluable (n = 57)

CD3 IHC-evaluable (n = 59)

Median age (range), years

56 (21‒88)

62 (31‒88)

62 (31‒88)

55 (27‒81)

Sex, n (%)

Male

114 (59)

30 (51)

29 (51)

31 (53)

Female

79 (41)

29 (49)

28 (49)

28 (47)

ECOG performance status,n (%)

0

86 (45)

32 (54)

31 (54)

23 (39)

1

106 (55)

27 (46)

26 (46)

36 (61)

Disease stage at diagnosis,n (%)

Stage I–III

107 (55)

33 (56)

33 (58)

29 (49)

Stage IV

86 (45)

26 (44)

24 (42)

30 (51)

Primary tumor location, n (%)

Colon NOS

3 (2)

2 (3)

2 (4)

0

Left-sided

60 (31)

25 (42)

24 (42)

19 (32)

Right-sided

130 (67)

32 (54)

31 (54)

40 (68)

Mutation status, n (%)

BRAF/KRAS wild type

60 (31)

15 (25)

15 (26)

17 (29)

BRAF mutation

42 (22)

11 (19)

11 (19)

9 (15)

KRAS mutation

71 (37)

27 (46)

25 (44)

24 (41)

Unknown

20 (10)

6 (10)

6 (11)

9 (15)

Clinical history of Lynch syndrome, n (%)

Yes

65 (34)

8 (14)

9 (16)

22 (37)

No

74 (38)

28 (47)

27 (47)

28 (47)

Unknown

54 (28)

23 (39)

21 (37)

9 (15)

BOR per INV, n (%)

CR

32 (17)

8 (14)

8 (14)

9 (15)

PR

74 (38)

26 (44)

24 (42)

19 (32)

SD

47 (24)

11 (19)

12 (21)

14 (24)

PD

33 (17)

11 (19)

11 (19)

13 (22)

NE

7 (4)

3 (5)

2 (4)

4 (7)

  1. aECOG performance status of 3: all treated, n = 1.
  2. bAll patients had stage IV disease at study entry. Source data are provided as a Source Data file. BOR best overall response, CD3 cluster of differentiation 3, CR complete response, ECOG Eastern Cooperative Oncology Group, IHC immunohistochemistry, INV investigator assessment, NE not evaluable, NOS not otherwise specified, ORR objective response rate, PD progressive disease, PR partial response, SD stable disease, WES whole-exome sequencing.