Introduction
Cholangiocarcinoma (CCA) is a tumor that arises from the epithelium of the bile ducts
and is the second most common type of liver cancer [1–3]. The incidence of CCA is increasing in many countries. The highest rates of CCA are found in northeastern Thailand due to
liver fluke infection [2–5]. In the United States, median overall survival is 8 and 4 months,
for patients with extrahepatic and intrahepatic CCA, respectively [6]. CCA is a lethal
malignancy due to its biologic aggressiveness, locally advanced disease at presentation and
high recurrence rate. The risk factors currently associated with CCA are heterogeneous, all
of which can induce cholestasis with chronic inflammation and pathophysiological aspects
underlying the development of CCA [7]. Chronic inflammation is responsible for the genesis of CCA by promoting cholangiocyte proliferation [8,9]. Indeed, chronic inflammation
leads to immune activation with the release of cytokines and growth factors that induce the
recruitment of immune cells and fibroblasts into the tissue microenvironment.
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