AASLD Abstracts Multivariate logistic regression analyses showed that younger age, African-American race, scirrhous, spindle cell or pleomorphic histology and severe fibrosis score were independent factors associated with AFP-elevated HCC. Conclusions: Elevated pretreatment serum AFP level (i.e. A-stage) is an AJCC-stage independent poor prognostic factor in HCC. We recom- mend the incorporation of A-stage within the current TNM-based AJCC staging system to enhance estimates of survival and aid therapeutic decision-making, especially in earlier stage HCC. Figure 1- Overall and Disease Specific Survival of AFP-Incorporated AJCC Stages for Hepato- cellular Carcinoma Mo1042 Incidence and Predictors of Lymph Nodal Metastases in Patients With Cholangiocarcinoma in the United States Katherine Shaffer, Sungjin Kim, Anthony M. Gamboa, Jennifer A. Luke, Sunil Dacha, Andrew B. Adams, Stuart J. Knechtle, Anjana Pillai, Kevin E. Woods, Steven Keilin, Qiang Cai, Zhengjia Chen, Field F. Willingham Background: Previously an exclusion criteria for orthotopic liver transplantation (OLT), cholangiocarcinoma is now being considered for transplant under specific protocols in centers in the United States. Early results suggest a favorable outcome with proper patient selection. In those meeting transplant guidelines, a critical question for listing or exclusion with unresectable perihilar cholangiocarcinoma involves the presence or absence of lymph node metastases (LNM). Methods: Data from the Surveillance Epidemiology and End Results (SEER) database was abstracted for patients with confirmed cholangiocarcinoma from 2004 to 2010. Including perihilar and non-perihilar tumors, a multivariate logistic regression model was employed to identify independent predictors of lymph node involvement. Consid- ering only perihilar tumors, a univariate model was examined to evaluate for predictors of LNM. Results: 14,186 patients with cholangiocarcinoma were evaluated, of which 6,403 patients had known LNM status. Of these, 1934 were perihilar and 4469 were non-perihilar. In a best predictive multivariate model including perihilar and non-perihilar tumors, grade and T stage were significantly and independently associated with LNM (p<0.001). On univariate modeling in patients with tumors at a perihilar location, AJCC stage [6] (p<0.001), grade (p<0.001), T stage (p<0.001), and tumor size (p=0.029) were significantly related to lymph node status. Gender and age at diagnosis approached but did not reach significance (p=0.070 and p=0.063 respectively). Neither the serum AFP level nor the degree of liver fibrosis (none to moderate versus severe fibrosis or cirrhosis) were significantly associated with LNM (p=0.840 and p=0.705, respectively). Patients with well differentiated tumors tend to have a negative lymph node. Those with T4 stage tumors were more likely to have a positive lymph node. Patients with smaller tumor size (0 - 1.9 cm) were much more likely to have negative LNM; however, 32.8% were nodal metastasis positive. Conclusion: For patients with perihilar cholangiocarcinoma, AJCC stage, the degree of differentiation, T stage, and tumor size were all significantly related to lymph node metastases while serum AFP level and the degree of liver fibrosis were not. While patients with small tumor sizes (<1.9cm) were much less likely to have nodal metastases, there was still a relatively high incidence of nodal spread, and therefore a thorough evaluation to detect nodal involvement prior to OLT is indicated. S-994 AASLD Abstracts Mo1043 Outcomes in Veterans With Hepatocellular Carcinoma (HCC) - A Single Center Experience Over 10 Years Amar Mahgoub, Thoetchai Peeraphatdit, Thomas J. Maust, Kelly McMaken, Astrid Knott, Paul Thuras, Eric Dieperink, Christine Pocha Purpose: Assess the long-term efficacy of treatment and related outcomes of patients with primary hepatocellular cancer (HCC). We investigated which patient and treatment related factors influence survival/mortality. Methods: Between 2000-2011, 234 patients were diag- nosed with HCC (ICD-9: 155.0) at the Minneapolis VA Health Care System. A retrospective chart review was conducted, demographic and clinical characteristics, treatment modality and outcome (all-cause mortality) were collected. Chi-Square and logistic regression were used to determine factors associated with mortality. Kaplan-Meier curves were constructed to estimate survival. Results: Of the 234 all male patients, mean age of 62.8, 81.2% were Caucasian, 52.2% had hepatitis C, and 65.8% had compensated liver disease with a mean MELD score of 9.8 at the time of HCC diagnosis. 60.7% (142/234) had Child Pugh A cirrhosis, 23.1% (54/234) B, 9.8% (23/234) C, and 6.4% (15/234) had missing data. All- cause mortality was 83.8% with a mean follow up time of 17.4 months. Most common co- morbidities were diabetes (36.3%), cardiac disease (28.6%), alcohol abuse (54.7%), substance use disorders (20.9%), and depression (29.5%), and but none increased all-cause mortality. 11.5% (27/234) of the patients received potential curative treatment including resection, liver transplantation, percutaneous ethanol injection (PEI) or radiofrequency ablation (RFA), 44.0% (103/234) received palliative treatment including trans-arterial chemoembolization (TACE), sorafenib, or body radiation, 14.1% (33/234) received both palliative and curative treatment and 30.3% (71/234) received no treatment. Median survival was 3 months in patients not receiving any therapy, 20 months in patients receiving curative therapy, 25 months for combined therapy, and 15 months for palliation, only ( Χ2=66.1, p<0.001). Patients with AFP levels greater than 20 ng/ml had higher mortality rates (87.6%) than those with AFP levels of 20 ng/ml or less (76.6%) [ Χ2=4.5, p=.034]. Conclusions: Only a quarter of patients received curative treatment for HCC. A substantial number of Veterans did not receive any therapy; possibly due to lack of treatment candidacy due to age, co- morbidities and more advanced liver disease despite all treatment options being available at the time of HCC diagnosis. Survival difference between the curative and palliative treatment group is less than one would expect which represent real life experience however warrants further investigation. Mo1044 Recruitment of Mast Cells Into the Tumor Microenvironment via c-KIT/Scf Increases Human Cholangiocarcinoma Proliferation and Angiogenesis Christopher Johnson, Sharon DeMorrow, Laura Hargrove, Lindsey Kennedy, Allyson B. Graf, Heather L. Francis BACKGROUND: Cholangiocarcinoma (CCA) growth is regulated by autocrine/paracrine signaling. The tumor microenvironment of CCA is composed of numerous cells including mast cells (MC). After activation, mast cells release numerous factors including histamine and VEGF, which increase tumor progression and angiogenesis. Cholangiocytes secrete the mast cell chemoattractant, stem cell factor (SCF), which functions via the mast cell growth factor receptor c-Kit. We have shown that (i) cholangiocytes express histidine decarboxylase (HDC) and secrete histamine; and (ii) HDC inhibition reduces CCA growth and VEGF expression via autocrine signaling. HYPOTHESIS: Recruitment of mast cells into the tumor microenvironment increases CCA growth. METHODS: We determined the presence of MCs in tumor sections stained with toluidine blue from nu/nu mice treated with NaCl, histamine or alpha-methyl-dl-histidine (HDC inhibitor) and in tumors composed of cells lacking HDC. The expression of c-kit, HDC and VEGF in these tumors was measured by qPCR. MC number and the expression of c-kit, chymase and tryptase were evaluated by immunohistochemistry in human CCA tissue arrays. In vitro, Mz-ChA-1 cells were treated with MC supernatants and proliferation and histamine secretion (by EIA) was measured. HDC, c-kit and VEGF expres- sion was measured by qPCR and immunoblots after stimulation with MC supernatants. Wound healing was performed in Mz-ChA-1 cells before and after treatment with MC supernatants. We performed migration/invasion assays using modified Boyden chambers loaded with Mz-ChA-1 cells and treated with BSA or the stem cell factor inhibitor, ISCK03 to determine if MC migration is dependent upon the c-kit/SCF interaction. RESULTS: In tumors from mice treated with histamine there was increased (i) MC number and (ii) HDC, c-kit and VEGF expression compared to vehicle-treatment. In mice that were treated with the HDC inhibitor or in tumors lacking HDC there were fewer MCs and decreased HDC, c-kit and VEGF expression compared to histamine or vehicle treatment. In tissue biopsies from patients with CCA there was increased (i) MC number and (ii) HDC, C-kit, chymase and tryptase expression. In vitro, stimulation with MC supernatants increased CCA prolifera- tion and histamine release as well as HDC, c-kit and VEGF expression. The addition of MC supernatants significantly increased Mz-ChA-1 wound closure and migration capacity compared to basal treatments. Inhibition of SCF in Mz-ChA-1 cells significantly inhibited the migration of MCs. CONCLUSION: MCs are recruited into the tumor microenvironment of CCA via c-kit/SCF and increase tumor progression and VEGF expression. Blocking MC migration into the tumor microenvironment may be important for CCA management. This work is supported by the PSC Partnership Foundation.