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. 2012;1(1):71-80.

Cholangiocarcinoma pathogenesis: Role of the tumor microenvironment

Dinorah Leyva-Illades, Matthew McMillin, Matthew Quinn, Sharon Demorrow

Cholangiocarcinoma pathogenesis: Role of the tumor microenvironment

Dinorah Leyva-Illades et al. Transl Gastrointest Cancer. 2012.

Abstract

Cholangiocarcinoma is a tumor that originates from the neoplastic transformation of the epithelial cells of the intrahepatic or extrahepatic bile ducts. This type of cancer is difficult to diagnose, extremely aggressive, and has very poor prognosis. It is also relatively resistant to chemotherapy and radiation therapy. Its pathogenesis is poorly understood, however it is known that the tumor microenvironment is a very important factor in the regulation of tumor angiogenesis, invasion, and metastasis. The current knowledge about the mechanisms by which these events are regulated as well as the role of the tumor microenvironment in the pathogenesis and classification of cholangiocarcinoma will be discussed.

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Conflict of interest statement

No potential conflict of interest.

Figures

Figure 1
Figure 1
Effects of stromal support cells on tumor growth and metastasis. B (B-cell), EMT (epithelial-mesenchymal transition), M (monocyte), T (T-cell), TAM (tumor associated macrophage).
Figure 2
Figure 2
Interactions between cholangiocarcinoma and angiogenic factors that regulate proliferation and angiogenesis. VEGF (vascular endothelial growth factor), FGF (fibroblast growth factor), EGF (epidermal growth factor).
Figure 3
Figure 3
Effects of signaling molecules secreted by cholangiocarcinoma-derived cancer-associated fibroblasts on cholangiocarcinoma progression. CAF (cancer-associate fibroblasts), HGF (hepatocyte growth factor), PDGF (platelet-derived growth factor), SDF-1 (stromal derived factor-1).
Figure 4
Figure 4
Differential activation of macrophages and their effect on tumor growth. M1 (pro-inflammatory), M2 (anti-inflammatory).
See this image and copyright information in PMC

References

    1. Alpini G, Prall R, LaRusso N. The pathobiology of biliary epithelia. In: Arias I, Boyer J, Chisari F, editors. The liver; biology and pathobiology. 4. Philadelphia: Lippincott Williams & Wilkins; 2001. pp. 421–35.
    1. Sirica AE. Cholangiocarcinoma: molecular targeting strategies for chemoprevention and therapy. Hepatology. 2005;41:5–15. - PubMed
    1. Patel T. Worldwide trends in mortality from biliary tract malignancies. BMC Cancer. 2002;2:10. - PMC - PubMed
    1. Ben-Menachem T. Risk factors for cholangiocarcinoma. Eur J Gastroenterol Hepatol. 2007;19:615–7. - PubMed
    1. Gores GJ. Cholangiocarcinoma: current concepts and insights. Hepatology. 2003;37:961–9. - PubMed

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