Figure 3
Correlation between KRAS mutational status and clinical features of patients. (a) Patients with a low KRASG12D/V amplicon (< 37 KRAS WT) had a significantly longer median OS duration than patients with a high (> 37 KRAS WT amplicon) KRAS WT amplicon; (b) copies of KRASG12D/V decreased after therapy and increased at progression time; (c,d) The patients not undergoing to resection surgery of the primary tumour have a number of KRASG12D/V copies higher compared to those who have undergone surgery; it’s the same for the fractional abundance parameter; (e,f) patients with positive expression of CEA have a number of KRASG12V/D copies and a fractional abundance higher than CEA negative patients; (g) fractional abundance in metastatic surgery patients according to CEA expression at basal and progression time point; (h) amount of KRAS WT according to size of tumor in metastatic surgery patients.
