1. Volume 54, Issue 5, Pages 1073-1078 (May 2011)
Epithelial-to-mesenchymal transition and acquired resistance to sunitinib in a patient with hepatocellular carcinoma 
Hélène Marijon, Safi Dokmak, Valérie Paradis, Magaly Zappa, Ivan Bieche, Mohamed Bouattour, Eric Raymond, Sandrine Faivre 
Journal of Hepatology 
Volume 54, Issue 5, Pages (May 2011)
DOI: /j.jhep
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2. Fig. 1
HCC tomodensitometric aspect at baseline (A), under anti-angiogenic treatment (B), and at progression (C). Lower images are schemes representing the tumor in green and necrosis in gray. Exposure to sunitinib was associated with occurrence of central tumor necrosis and regrowth from peripheral part of the tumor at the time of progression.
Journal of Hepatology  , DOI: ( /j.jhep )
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3. Fig. 2
Pathological analysis at the time of progression under sunitinib. Macroscopic examination (A) showed heterogeneous tumor with fleshy beige areas associated with cholestatic, necrotic, and hemorrhagic areas. Microscopic examination identified one component made by well- to moderately-differentiated HCC (B) and one component made by sarcomatoïd-like cells (C).
Journal of Hepatology  , DOI: ( /j.jhep )
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4. Fig. 3
Proteins (immunohistochemistry) and mRNA (qRT-PCR) expressions of biomarkers in the carcinoma and the mesenchymal components of a hepatocellular carcinoma at the time of sunitinib progression. (A) Cells in both components expressed strong α-FP immunostainings. The well-differentiated carcinoma component expressed E-cadherin and did not express vimentin, while the mesenchymal section displayed no E-cadherin expression and a strong vimentin immunostaining. (B) mRNA of S100A4, Claudin 4, and MUC1 were down regulated in both tumor components compared to adjacent liver, whereas Ki67 and HMGA2 were up-regulated. mRNA of N-cadherin remained unchanged.
Journal of Hepatology  , DOI: ( /j.jhep )
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