Key result
Angiotensin-II receptor density was markedly down-regulated in hepatic tumors compared with normal or cirrhotic liver.
Observational (n=18)
May inform angiotensin-II targeting strategies in hepatic tumors; leaves open clinical translation from in vitro data alone.
OBJECTIVE: To characterize angiotensin-II receptor density and affinity in normal and cirrhotic livers and in hepatocellular and metastatic colorectal cancer. SUMMARY BACKGROUND DATA: Several studies have indicated a possible beneficial effect of angiotensin-II as a biologic response modifier in the treatment of hepatic or metastatic colon cancer. This is based on evidence that angiotensin-II will cause a selective increase in arterial vasoconstriction in normal liver compared with tumor. METHODS: Human hepatoma (5), metastatic colon (10), or cirrhotic (3) liver was obtained. Non-tumor-bearing regions served as normal liver. Angiotensin-II receptor binding was determined on membranes with 125I-angiotensin-II and in situ studies were performed using the biotin-avidin detection system. RESULTS: Angiotensin-II receptor density was markedly down-regulated in tumor compared with normal or cirrhotic liver. CONCLUSIONS: A loss of angiotensin-II receptors occurs on the neovasculature of hepatic tumors.
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Sitzmann et al. (1994) conducted an observational in Hepatocellular and metastatic colorectal cancer (n=18). Hepatic tumors (hepatoma and metastatic colon cancer) vs. Normal or cirrhotic liver was evaluated on Angiotensin-II receptor density. Angiotensin-II receptor density was markedly down-regulated in hepatic tumors compared with normal or cirrhotic liver.
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