Somatostatin receptors in resected hepatocellular carcinoma: status and correlation with markers of poor prognosis

Abstract

Membrane SSTR2 is detected reliably in HCCs by IHC, and is a potential therapeutic target, as it is coexpressed with markers of poor prognosis.

Hepatocellular Carcinoma Mimicking Neuroendocrine Tumor Metastasis on 68Ga-DOTATATE PET/CT

“…Immunohistochemistry studies have documented membrane SSRs in more than one-third of HCCs, most commonly SSR2. 3 Prior somatostatin scintigraphy of advanced HCC similarly demonstrated uptake in approximately one-third of primary HCC tumors. 4 Somatostatin receptor expression in HCC has led to the application of somatostatin analogs for the treatment of HCC with mixed success.…”

Treatment of Advanced Hepatocellular Carcinoma with Somatostatin Analogues: A Review of the Literature

“…Reubi et al were the first authors to demonstrate the presence of SSTRs in HCC [9]. We and others have confirmed several years ago that different subtypes of SSTRs are expressed in human cirrhosis and HCC [10,11,12,13,14,15]. Even if most SSTR subtypes have been shown to be present in HCC, there is high variability in expression in the different studies.…”

“…Patient populations and type of treatment were diverse in the different trials, but probably more important is the presence of SSTRs and SSTR subtype expression in the tumor and surrounding tissue. Indeed, only 40–70% of the HCCs express SSTRs, of which not all express SSTR subtypes 2, 3 or 5 for which the synthetic SST analogues have affinity [9,10,11,12,13,14,15]. It makes no sense to treat patients with SST analogues if the tumor does not express SSTRs at all, or only SSTRs for which the SST analogue has no or low affinity.…”

“…Even if most SSTR subtypes have been shown to be present in HCC, there is high variability in the expression in the different studies. The expression of SSTR subtypes 1, 2, 3 and 5 in HCC cell lines and tumor tissue ranged from 46–76%, 30%–67%, 0–64%, and 0–76% respectively [9,10,11,12,13,14,15]. The reason for variability might be differences in tumor biology, but also different techniques to demonstrate SSTR expression.…”

“…The reason for variability might be differences in tumor biology, but also different techniques to demonstrate SSTR expression. Moreover, SSTR expression was correlated with markers of poor prognosis [11]. Indeed, SSTR2 membrane staining was associated with high AFP levels, poor differentiation, and CK19 expression, all of which are predictors of poor survival.…”