{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T06:30:17Z","timestamp":1778567417486,"version":"3.51.4"},"reference-count":105,"publisher":"MDPI AG","issue":"2","license":[{"start":{"date-parts":[[2026,1,26]],"date-time":"2026-01-26T00:00:00Z","timestamp":1769385600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["CIMB"],"abstract":"<jats:p>Growth factors play a significant role in the immunopathogenesis of liver diseases, especially liver cirrhosis and hepatocellular carcinoma (HCC). The somatostatin analog octreotide has been used as treatment in advanced HCC, based on its anti-neoplastic effects in vitro. Therefore, the effect of somatostatin and octreotide was studied on several growth factors in patients with HCC. Nineteen patients with advanced HCC were treated with octreotide and compared with thirty-seven patients with viral cirrhosis (19 decompensated) treated with intravenous somatostatin for severe bleeding from portal gastropathy. Five growth factors, namely Gastrin, Insulin-like growth factor 1 (IGF 1), Hepatocyte growth factor (HGF), Stem cell factor (SCF) and Vascular endothelial growth factor (VEGF) were measured in serum before and after treatment with specific commercially available ELISAs. Seventeen healthy individuals and nineteen patients with chronic viral hepatitis C (CAH) were used as pre-treatment controls. Eighteen patients with advanced Primary Biliary Cholangitis (stage III and IV) before and after Ursodeoxycholic acid (UDCA) treatment were also studied. Pre-treatment levels of Gastrin were significantly increased in HCC, cirrhosis and PBC but not in CAH. Levels were significantly reduced by octreotide or somatostatin but also by UDCA in PBC. By contrast, IGF1 showed a mirror image being significantly reduced in HCC, cirrhosis and PBC, but not in CAH. Post-treatment levels were reduced in all groups, but not in PBC. Levels of HGF were significantly increased in HCC and cirrhosis but not in CAH and PBC. They were further increased in HCC after treatment. SCF increased only in HCC and was reduced after octreotide but not after somatostatin treatment. VEGF was reduced in cirrhosis and CAH but not in PBC. It was not significantly increased in HCC, but it was reduced by octreotide and was increased after UDCA. In this retrospective observational study, somatostatin and its analog octreotide have a significant effect on several growth factors involved in HCC pathogenesis.<\/jats:p>","DOI":"10.3390\/cimb48020134","type":"journal-article","created":{"date-parts":[[2026,1,26]],"date-time":"2026-01-26T12:41:16Z","timestamp":1769431276000},"page":"134","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Somatostatin Effect on Growth Factors in Hepatocellular Carcinoma"],"prefix":"10.3390","volume":"48","author":[{"given":"Angeliki","family":"Tsakou","sequence":"first","affiliation":[{"name":"1st Department of Internal Medicine, AHEPA University Hospital, 54621 Thessaloniki, Macedonia, Greece"},{"name":"Laboratory of Gastroenterology and Hepatology, School of Medicine, University of Crete, Voutes Campus, 70013 Heraklion, Crete, Greece"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2506-5252","authenticated-orcid":false,"given":"George","family":"Notas","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Endocrinology, School of Medicine, University of Crete, Voutes Campus, 70013 Heraklion, Crete, Greece"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-7068-4570","authenticated-orcid":false,"given":"Costantinos","family":"Xidakis","sequence":"additional","affiliation":[{"name":"Laboratory of Gastroenterology and Hepatology, School of Medicine, University of Crete, Voutes Campus, 70013 Heraklion, Crete, Greece"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8595-2750","authenticated-orcid":false,"given":"Ioannis","family":"Tsomidis","sequence":"additional","affiliation":[{"name":"Laboratory of Gastroenterology and Hepatology, School of Medicine, University of Crete, Voutes Campus, 70013 Heraklion, Crete, Greece"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6875-906X","authenticated-orcid":false,"given":"Elias","family":"Kouroumalis","sequence":"additional","affiliation":[{"name":"Laboratory of Gastroenterology and Hepatology, School of Medicine, University of Crete, Voutes Campus, 70013 Heraklion, Crete, Greece"},{"name":"Department of Gastroenterology, University General Hospital of Heraklion (PAGNH) School of Medicine, University of Crete, 71500 Heraklion, Crete, Greece"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Argyro","family":"Voumvouraki","sequence":"additional","affiliation":[{"name":"1st Department of Internal Medicine, AHEPA University Hospital, 54621 Thessaloniki, Macedonia, Greece"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2026,1,26]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"9","DOI":"10.1007\/s00535-013-0907-x","article-title":"The EGFR signalling system in the liver: From hepatoprotection to hepatocarcinogenesis","volume":"49","author":"Berasain","year":"2014","journal-title":"J. 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