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. 2016 Nov 25;35(1):97.
doi: 10.1186/s40880-016-0162-7.

Implications of vessel co-option in sorafenib-resistant hepatocellular carcinoma

Elizabeth A Kuczynski  1 , Robert S Kerbel  2
Affiliations

Implications of vessel co-option in sorafenib-resistant hepatocellular carcinoma

Elizabeth A Kuczynski et al. Chin J Cancer. .

Abstract

The reason why tumors generally have a modest or transient response to antiangiogenic therapy is not well understood. This poses a major challenge for sorafenib treatment of advanced hepatocellular carcinoma (HCC) where alternate therapies are lacking. We recently published a paper entitled "Co-option of liver vessels and not sprouting angiogenesis drives acquired sorafenib resistance in hepatocellular carcinoma" in the Journal of the National Cancer Institute, providing a potential explanation for this limited benefit. We found that in mice bearing HCCs that had acquired resistance to sorafenib, tumors had switched from using angiogenesis for growth to co-opting the liver vasculature by becoming more invasive. Accumulating evidence suggests that many human tumor types may use vessel co-option, which has profound implications for the use of anti-angiogenic agents for cancer treatment.

Keywords: Hepatocellular carcinoma; Non-angiogenic; Resistance; Sorafenib; Vessel co-option.

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Figures

Fig. 1
Fig. 1
Proposed mechanism of acquired resistance to the multikinase inhibitor sorafenib in hepatocellular carcinoma (HCC). Highly angiogenic HCCs are initially responsive to sorafenib treatment. Over time, tumor cells become more invasive which promotes co-option of liver vessels in the face of angiogenesis blockade. EMT epithelial-to-mesenchymal transition
See this image and copyright information in PMC

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