title: The combination of HTATIP2 expression and microvessel density predicts converse survival of hepatocellular carcinoma with or without sorafenib.
abstract: Our previous studies have demonstrated that sorafenib can promote the dissemination of hepatocellular carcinoma (HCC) through downregulation of HTATIP2, a suppressor of tumor growth and metastasis that is associated with inhibition of angiogenesis. Here, we investigated the predictive values of the HTATIP2 level and microvessel density (MVD) with or without sorafenib administration for HCC. Three independent cohorts were included. Using tissue microarray, we assessed the relationship between HTATIP2 expression/MVD and overall survival. The results showed that high HTATIP2 expression and a low MVD value were independent protective prognostic factors after curative HCC resection (297 cases/cohort 1); however, both parameters were converted to independent negative prognostic indicators for patients with postsurgical sorafenib treatment (69/143 cases/cohort 2; P<0.05 for all). This same relationship was observed in patients that received sorafenib treatment for advanced HCC (83 cases/cohort 3; efficacy measures and survival analyses, P<0.05 for all). Moreover, the combination of HTATIP2 and MVD had better power to predict patient death and disease recurrence (P<0.001 for both). We conclude that the combination of HTATIP2 and MVD predicts the converse survival of HCC with or without sorafenib intervention. Our findings can assist in the selection of candidates for personalized treatment with sorafenib.
authors.affiliation: Department of Pancreatic and Hepatobiliary Surgery, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University; and Pancreatic Cancer Institute, Fudan University, Shanghai, China.
authors.forename: Wen-Quan
authors.initials: WQ
authors.lastname: Wang
authors.forename: Liang
authors.initials: L
authors.lastname: Liu
authors.forename: Hua-Xiang
authors.initials: HX
authors.lastname: Xu
authors.forename: Hui-Chuan
authors.initials: HC
authors.lastname: Sun
authors.forename: Chun-Tao
authors.initials: CT
authors.lastname: Wu
authors.forename: Xiao-Dong
authors.initials: XD
authors.lastname: Zhu
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.forename: Jin
authors.initials: J
authors.lastname: Xu
authors.forename: Chen
authors.initials: C
authors.lastname: Liu
authors.forename: Jiang
authors.initials: J
authors.lastname: Long
authors.forename: Quan-Xing
authors.initials: QX
authors.lastname: Ni
authors.forename: Zhao-You
authors.initials: ZY
authors.lastname: Tang
authors.affiliation: Department of Pancreatic and Hepatobiliary Surgery, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University; and Pancreatic Cancer Institute, Fudan University, Shanghai, China.
authors.forename: Xian-Jun
authors.initials: XJ
authors.lastname: Yu
mesh_terms: D000123:Acetyltransferases / Q000096:biosynthesis*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D006528:Carcinoma, Hepatocellular / Q000098:blood supply / Q000188:drug therapy* / Q000378:metabolism; D005260:Female; D006801:Humans; D008113:Liver Neoplasms / Q000098:blood supply / Q000188:drug therapy* / Q000378:metabolism; D008297:Male; D055806:Microvessels / Q000473:pathology; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000188:drug therapy / Q000378:metabolism; D009536:Niacinamide / Q000031:analogs & derivatives* / Q000627:therapeutic use; D010671:Phenylurea Compounds / Q000627:therapeutic use*; D011379:Prognosis; D000077157:Sorafenib; D014157:Transcription Factors / Q000096:biosynthesis*; D055815:Young Adult
chemical_list: D000970:Antineoplastic Agents; D010671:Phenylurea Compounds; D014157:Transcription Factors; D009536:Niacinamide; D000077157:Sorafenib; D000123:Acetyltransferases; C111246:HTATIP2 protein, human