Abstract 5539: An integrated multidisciplinary approach for prediction of HCC development in patients with liver disease utilizing genomics, elastography, imaging and circulating tumor cells
Authors: Thomas Emmanuel , Schiff Eugene , Kwon Deukwoo , Madrazo Beatrice 
Published: August 2018

Abstract
Background: HCV induced HCC is higher in minority populations. To serve these communities, it is imperative that we understand the genetic and cellular based mechanisms underpinning the linkages between HCV and HCC. The aims of our study were to assess changes in transient elastography (TE) and fibrosis-4 (FIB-4) score in patients with chronic hepatitis C (CHC) in a large cohort of patients. Patients were also stratified for HCC risk based on genomic and imaging data with inclusion of screening for circulating tumor cells. Methods: Our cohort included 1,400 patients and approximately 500 had liver biopsies. Our retrospective prospective study included 60 patients with CHC and a baseline liver biopsy who achieved SVR after treatment with DAA regimens and had a pretreatment TE study and at least one follow up TE measurement at 24 weeks or later post end of treatment response (EOTR). The estimated stage of liver fibrosis based on TE was categorized as F0-F2 (&lt;9.4kpa), or F3 (9.5 - 12.4 Kpa), or F4/cirrhotics (TE &gt;12.5 kpa). Results: Approximately 1,400 patients were successfully assessed by fibroscan and comparisons made with clinical parameters of liver disease. The median baseline TE for the 60 patients who achieved SVR was 11.9 Kpa (range 3.8 to 65.2) and at follow up, TE decreased to 7.35 Kpa (range 2.9 to 34.8) with a median change in TE of -3.4 Kpa (range -35.3 to +1, p=7.355e- 11). Follow up median TE done in the cirrhotic population after median time of 39 weeks post EOTR decreased to 11.7 Kpa and FIB4 was 2.3. The median change of TE in cirrhotic patients was -6.5 kpa (range -35.3 to +1, p=1.043e-7) and for FIB4 was -1.97 (range -17.47 to -0.33, p=1.49e-8). Non-cirrhotic patients (TE&lt;12.4) comprised 55% of the entire cohort and their median change of TE was -2.4 Kpa (range -6.4 to 0.7, p=1.539e-6) and FIB4 was -0.68 (range -2.8 to 0.41, p=2.987e-6). 48% of the entire cohort down-staged their liver fibrosis as determined by TE. In a multiple logistic regression analysis for factors associated with down-staging in liver fibrosis, we found that patients who were treatment naïve were more likely to improve their fibrosis stage (OR 5.73, p=0.033). Conclusions: Liver fibrosis stage, as determined by TE, improved after achieving SVR with DAA treatments in most patients. Although cirrhotic patients had a more significant drop in their median TE when compared to non-cirrhotic patients, they had a lower probability of improving their fibrosis stage and maintained a continued risk to develop HCC. In addition, we identified a group of patients whose TE score did not improve post SVR also representing a cohort of patients whose HCC risk remained. The patients who remain at risk for HCC will be further stratified for increased propensity to develop HCC utilizing genomics, advanced imaging and screening for circulating tumor cells.
Citation Format: Emmanuel Thomas, Eugene Schiff, Deukwoo Kwon, Beatrice Madrazo. An integrated multidisciplinary approach for prediction of HCC development in patients with liver disease utilizing genomics, elastography, imaging and circulating tumor cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 5539.