After 3 years, the index Rachmilevitz in group 1 was 3,3 ± 0,4 points, the 2nd – 5,3 ± 0,4 points (p < 0,001), the index of Mayo in group 1 was 2.9 ± 0,3 points in the second Sorafenib price – 4,1 ± 0,34 (p < 0,001). After 4 years – index Rachmilevitz in group 1 was 3,5 ± 0,4 points, the 2nd – 5,7 ± 0,4 points (p < 0,001), the index of Mayo in group 1 was 3, 2 ± 0,35 points in the second – 4,6 ± 0,28 (p < 0,001). After 5 years – Rachmilevitz index in group 1 was 4,6 ± 0,4 points, the 2-nd – 6,0 ± 0,34 points (p < 0,001), the index of Mayo in group 1 was 4, 0 ± 0,37 points in the second – 4,7 ± 0,28 (p < 0,001). In the first group of patients in

remission at 1, 2, 3, 4, and 5 years was kept at 75,8% (n = 44), 68,9% (n = 40), 60,3% (n = 35), 58, 6% (n = 34) and 44,8% (n = 25) of patients, respectively. In the second group of patients at 1, 2, 3, 4, and 5 years in remission persisted in 34,0% (n = 17), 28,0% (n = 14), 22,0% (n = 11), 14,0% (n = 7) and 10,0% (n = 5) patients, respectively. Over the entire period of observation Rapamycin in any case there were no malignant transformation of life-threatening

infectious complications and death. Conclusion: MSC transplantation reduces inflammatory activity and maintaining a long-term clinical and endoscopic remission in patients with ulcerative colitis compared with therapy 5-ASA/GCS. Key Word(s): 1. stromal cells; 2. ulcerative colitis; 3. mesenchymal; Presenting Author: JIE LIANG Additional Authors: KAICHUN WU, DAIMING FAN Corresponding Author: JIE LIANG Objective: Chronic inflammation is now recognized to have decisive roles in the pathogenesis of cancer. Inflammatory bowel diseases (IBD) are a salient example of the link between chronic inflammation Tau-protein kinase and cancer and one of the consequences of persistent inflammation of the colon or ulcerative colitis (UC) is an increased risk for developing colorectal cancer. However, the mechanism is not fully understood. Methods: Animal model was used for colits and colits-associated colon cancer

study. Immunohistochemistry, Western blot and FACS analysis were used for mechanism investigation. Results: We show that sphingosine-1-phosphate (S1P) produced by upregulation of sphingosine kinase 1 (SphK1) links chronic intestinal inflammation to colitis-associated cancer (CAC) and both are exacerbated by deletion of SphK2. S1P is essential for production of the multifunctional NF-κB-regulated cytokine IL-6, persistent activation of the transcription factor Stat3, and consequent upregulation of the S1P receptor, S1PR1. The pro-drug FTY720 decreased SphK1 and S1PR1 and eliminated the NF-κB-IL-6-Stat3 amplification cascade and development of CAC even in SphK2−/− mice and may be useful in treating colon cancer in individuals with ulcerative colitis. Conclusion: SphK1-S1P-S1PR1 axis is at the nexus between NF-κB and Stat3 and connects chronic inflammation and CAC. Key Word(s): 1. S1P; 2.