03:09 PM Abstract No. 326 Effectiveness of drug-eluting bead transarterial chemoembolization (DEB-TACE) and radioembolization (TARE) for patients with wild-type KRAS and mutant KRAS status

To compare tumor response and survival of KRAS wild-type and KRAS mutation patients with colorectal liver metastases (CRLM) treated with DEB-TACE and TARE. Retrospective review of patients who underwent transarterial therapy, DEB-TACE (loaded with irinotecan or doxorubicin) or TARE (glass or resin particles), with documented KRAS mutation status at a single U.S. academic medical center. Student’s t-tests, Fisher’s exact and Chi-square tests were used to compare groups. Kaplan-Meier and Cox regression were performed to assess overall survival (OS) and progression free survival (PFS). 65 and 66 patients had documented KRAS mutant and wild-type pathology respectively. KRAS mutation cohort had more > 10 liver lesions (75.4% vs 53.0%, p = 0.017), and extra hepatic metastases (64.6% vs 45.5%, p = 0.028) than the wild-type cohort. Otherwise, both groups had similar background variables. Both groups had similar all-grade and high-grade adverse events after transarterial treatment. Overall RECIST tumor response rate for KRAS wild-type and KRAS mutant was 15.5% and 6.0% (p = 0.29) respectively. KRAS mutation cohort had worse median OS at 10.0 months [95% CI- 7.5, 12.5 months] vs 14.0 months [95% CI- 10.4, 17.5 months] (p = 0.031). Median OS for KRAS mutation patient cohort treated with TARE was 10.0 months [95% CI- 7.4, 12.6 months] versus 14.0 months [95% CI- 11.0,17.0 months] (p = .14). Median OS for KRAS mutation patient cohort treated with DEB-TACE was 5.0 months [95% CI- 3.5, 6.5 months] versus 15.0 months [95% CI- 6.3, 23.7 months] (p = 0.17). With regression analysis, KRAS mutation status was not revealed as an independent prognostic factor for PFS (HR- 1.07 [.68, 1.7], p = .78) or OS (HR- 1.3 [.85, 2.0], p = .23). Compared to KRAS wild-type, KRAS mutation patient cohort had worse outcomes after transarterial therapy for CRLM. However, in this study KRAS mutation status was not found to be an independent prognostic factor for OS. Other tumor biological factors or background variables may be contributing to the differences observed.