Table 1.

Patient characteristics and KRAS mutation status. Gender, age, biopsy site, type of treatment institution, and KRAS mutation status are given across all patients (total columns) and in groups based on disease burden at the time of the biopsy used for the multiomic profiling described in this study (metastatic; locally advanced, unresectable [LAPC], or resected).

Disease status
Total (n = 640)Metastatic (n = 458)LAPC (n = 137)Resected (n = 45)
Gender
 Male328 (51%)245 (53%)70 (51%)13 (29%)
 Female312 (49%)213 (47%)67 (49%)32 (71%)
Age, years
 <5059 (9%)41 (9%)13 (9%)5 (11%)
 50–59165 (26%)124 (27%)28 (20%)13 (29%)
 60–69279 (44%)196 (43%)60 (44%)23 (51%)
 ≥70137 (21%)97 (21%)36 (26%)4 (9%)
Tumor biopsy site
 Liver259 (40%)258 (56%)1 (1%)0 (0%)
 Pancreas207 (32%)38 (8%)125 (91%)44 (98%)
 Lung41 (6%)41 (9%)0 (0%)0 (0%)
 Peritoneum57 (9%)57 (12%)0 (0%)0 (0%)
 Other76 (12%)64 (14%)11 (8%)1 (2%)
Treatment setting
 High volume414 (65%)309 (67%)77 (56%)28 (62%)
 Community practice226 (35%)149 (33%)60 (44%)17 (38%)
KRAS statusa
 Mutated535 (87%)385 (88%)115 (86%)35 (80%)
 WT, nonadenocarcinoma histologyb32 (5%)21 (5%)5 (4%)6 (14%)
 WT, other MAPK pathway alterationc11 (2%)9 (2%)1 (1%)1 (2%)
 WT, other histology and other MAPK5 (1%)2 (0.5%)3 (2%)0 (0%)
 True KRAS WT35 (6%)23 (5%)10 (7%)2 (4%)
  • aKRAS status by NGS was available in 618 of 640 patients.

  • bNonductal adenocarcinoma histologies included neuroendocrine, acinar cell, and ampullary.

  • cOther MAPK pathway alterations included NRAS amplification/mutation and BRAF mutation.