Efficacy of lanreotide in preventing the occurrence of chemically induced hepatocellular carcinoma in rats

Hepatocellular carcinoma (HCC) is increasing worldwide and is the third cause of cancer-related death. HCC develops in a pre-neoplastic organ, the cirrhotic liver. Therefore, chemoprevention could play a role in the management of HCC. We have previously shown that lanreotide, a somatostatin analogue...

Full description

Saved in:
Bibliographic Details
Published in:Chemico-biological interactions 2010-01, Vol.183 (1), p.238-248
Main Authors: Borbath, Ivan, Leclercq, Isabelle A., Sempoux, Christine, Abarca-Quinones, Jorge, Desaeger, Christine, Horsmans, Yves
Format: Article
Language:English
Subjects:
Alanine Transaminase - blood
Animals
Antineoplastic Agents - therapeutic use
Cell Proliferation
Diethylnitrosamine - toxicity
Fibrosis
Hepatocellular carcinoma
Liver Neoplasms, Experimental - chemically induced
Liver Neoplasms, Experimental - pathology
Liver Neoplasms, Experimental - prevention & control
Male
Peptides, Cyclic - therapeutic use
Prevention
Proliferation
Rats
Rats, Wistar
Receptors, Somatostatin - metabolism
Somatostatin - analogs & derivatives
Somatostatin - therapeutic use
Somatostatin analogue
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Hepatocellular carcinoma (HCC) is increasing worldwide and is the third cause of cancer-related death. HCC develops in a pre-neoplastic organ, the cirrhotic liver. Therefore, chemoprevention could play a role in the management of HCC. We have previously shown that lanreotide, a somatostatin analogue, inhibits the development of “foci of altered hepatocytes”, which represent very early neoplastic changes in rat liver. Here we induced bona fide HCC by means of a different chemically induced model that is known to lead to significant fibrosis before HCC appearance. Lanreotide was given from the beginning of the experiment in one group and from the time when significant fibrosis was present in the second group. Lanreotide decreased the frequency of occurrence of HCC in both groups. In both groups, significant decreases in hepatocyte proliferation and inhibition of fibrosis were demonstrated. When given at the start of the experiment, lanreotide dramatically decreased levels of angiogenic factors and enhanced apoptosis. Further work on the anti-tumoral effect of lanreotide is called for to assess the mechanistic relationships of its anti-proliferative and anti-angiogenic actions on liver neoplastic cells.
ISSN:0009-2797
1872-7786
DOI:10.1016/j.cbi.2009.10.011