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. 2020 May 29;27(9):3488–3497. doi: 10.1245/s10434-020-08657-6

Table 1.

Clinical characteristics of mixed response group

MR–R (n = 36) MR–NR (n = 22) p value
Median age 67 (29–85) 75 (48–85) 0.03
ECOG
 < 1 28 (78) 12 (55) 0.06
 ≥ 1 8 (22) 10 (45)
Gender
 Female 10 (28) 4 (18) 0.53
 Male 26 (72) 18 (82)
Location primary
 Trunk 8 (22) 6 (27) 0.55
 Lower ex 9 (28) 7 (32)
 Head/neck 10 (28) 3 (14)
 Penis NA 1 (5)
 Vulva/vaginal 1 (3) 2 (9)
 Unknown 7 (19) 3 (14)
Tumor histology
 SSM 7 (19) 5 (23) 0.76
 Nodular 9 (25) 4 (18)
 Acral NA 1 (5)
 Mucosal 1 (3) NA
 Desmoplastic 1 (3) NA
 Unknown 18 (50) 12 (54)
Ulceration
 No 12 (33) 8 (36) 0.99
 Yes 13 (36) 8 (36)
 Unknown 11 (31) 6 (27)
Median Breslow (mm) 4.1 (0.4–8.3) 3.2 (0.7–42) 0.64
M stage
 M1a 5 (14) 1 (5) 0.39
 M1b 11 (31) 2 (9) 0.1
 M1c 12 (33) 6 (27) 0.77
 M1d 7 (19) 13 (59) < 0.01
No. sites mets
 No 25 (69) 6 (27) < 0.01
 Yes 11 (31) 16 (73)
Mutational status
 BRAF V600E/K 14 (39) 4 (18) 0.05
 NRAS 7 (19) 8 (36) 0.41
 WT 7 (19) 8 (36) 0.53
 Not tested 3 (8) NA 0.27
 Total mutations ≥ 5 7 (19) 3 (14) 0.48
Median LDH 183 (148–213) 212 (190–247) < 0.01

MR–R mixed response to response, MR–NR mixed response to non-response, ECOG Eastern Cooperative Oncology Group, SSM sustained mixed response, BRAF V600E/K B-Raf proto-oncogene V600E/K mutation, NRAS NRAS proto-oncogene, WT wild type, LDH lactate dehydrogenase

Bold values indicate p < 0.05

Patients with a subsequent response tended to be younger (p = 0.03), were less likely to have M1d disease (p < 0.01), had fewer that 3 sites of metastases (p < 0.01), were more likely to have a BRAF V600E/K mutation (p = 0.05), and were less likely to have an elevated LDH (p < 0.01)