Programmed death-ligand 1 is upregulated in intrahepatic lymphoepithelioma-like cholangiocarcinoma
Metrics: PDF 923 views | HTML 1945 views | ?
Lei Wang1,2,*, Hui Dong3,*, Shujuan Ni1,2, Dan Huang1,2, Cong Tan1,2, Bin Chang1,2, Weiqi Sheng1,2
1Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China
2Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China
3Department of Pathology, Shanghai Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai, 200438, China
*These authors contributed equally to this work
Weiqi Sheng, email: email@example.com
Keywords: intrahepatic cholangiocarcinoma, intrahepatic lymphoepithelioma-like cholangiocarcinoma, clinicopathological characteristics, PD-L1, clinical outcomes
Received: May 10, 2016 Accepted: September 02, 2016 Published: September 10, 2016
Intrahepatic lymphoepithelioma-like cholangiocarcinoma (LELCC) is a rare variant of cholangiocarcinoma. Here, we report the largest single series of LELCC cases yet studied (n = 13). We retrospectively analyzed the clinical data of the 13 patients and measured the expression of programmed death-ligand 1 (PD-L1) in tumors using immunohistochemical staining. We also analyzed 15 cases of conventional intrahepatic cholangiocarcinoma (IHCC) for comparison. We found that eight patients with LELCC were infected with Epstein-Barr Virus (EBV), and EBV infection correlated with poor prognosis in LELCC. Four patients among the five (80.0%) without EBV had a history of chronic viral hepatitis B. None of the 15 cases of conventional cholangiocarcinoma were positive for EBV. PD-L1 was expressed in both the tumor cells and tumor-infiltrating immune cells in LELCC patients at higher levels than in IHCC patients (P < 0.05). These observations suggest that EBV infection may promote the development of LELCC, and that PD-L1 may be a potential therapeutic target for treatment of EBV-associated LELCC.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.