Somatostatin receptor subtype 5 (SSTR5) mRNA expression is related to histopathological features of cell proliferation in insulinomas

Endocr Relat Cancer. 2006 Mar;13(1):69-78. doi: 10.1677/erc.1.00962.

Abstract

Insulinomas are rare endocrine neoplasias that constitute the most frequent islet cell tumours. Somatostatin (SST) analogs are tentatively used to inhibit insulin secretion and control tumour growth in patients with local invasion or inoperative metastasis, but variable responses have been reported. Data regarding somatostatin receptor (SSTR) subtypes expression in insulinomas are conflicting. In this study, we evaluated 16 cases of primary insulinomas (including four primary plurihormonal tumours) and two hepatic metastases. Histopathological and immunohistochemical analysis for some features associated with tumour aggressiveness and semi-quantitative RT-PCR for SSTR1-5 and real-time qPCR for SSTR5 were performed. SSTR subtypes 1, 3, and 5 were expressed in 100%, SSTR2 in 89%, and SSTR4 only in 22% of the insulinomas. SSTR5 mRNA was positively correlated with histopathological features related to tumour aggressiveness (large tumour diameter, well-differentiated endocrine tumour with uncertain behaviour and higher number of cells with nuclear atypia). SSTR5 mRNA expression in primary insulinomas was lower than in primary plurihormonal tumours (P < 0.05). The observed positive correlation between SSTR5 expression and tumour size suggests that the use of SST analogues more specific to SSTR5 in the treatment of insulinomas deserves attention.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoma, Islet Cell
  • Adolescent
  • Adult
  • Aged
  • Cell Proliferation*
  • Female
  • Humans
  • Insulinoma / genetics
  • Insulinoma / metabolism
  • Insulinoma / pathology*
  • Liver Neoplasms / genetics
  • Liver Neoplasms / metabolism
  • Liver Neoplasms / secondary
  • Male
  • Middle Aged
  • Pancreatic Neoplasms / genetics
  • Pancreatic Neoplasms / metabolism
  • Pancreatic Neoplasms / pathology*
  • Pituitary Hormones / metabolism
  • Pituitary Neoplasms / genetics
  • Pituitary Neoplasms / metabolism
  • RNA, Messenger / metabolism*
  • Receptors, Somatostatin / genetics*
  • Receptors, Somatostatin / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • Pituitary Hormones
  • RNA, Messenger
  • Receptors, Somatostatin
  • somatostatin receptor 5