Expression of estrogen-induced genes and estrogen receptor β in pancreatic neuroendocrine tumors: implications for targeted therapy

Pancreas. 2014 Oct;43(7):996-1002. doi: 10.1097/MPA.0000000000000203.

Abstract

Objective: The indolent nature and expression of progesterone receptor (PR), a well-known estrogen-induced gene, in a subset of pancreatic neuroendocrine tumors (PanNETs), raise the possibility of hormonal regulation in these tumors.

Methods: Immunohistochemical expression of estrogen receptors (ERs) α and β as well as messenger RNA expression of estrogen-induced genes (PR, EIG121, IGF-1, IGF-1R, sFRP1, and sFRP4) by quantitative reverse transcription-polymerase chain reaction were examined in 131 World Health Organization grade G1 and G2 PanNETs and correlated their expression with clinicopathological features.

Results: Thirty-nine PanNETs (30%) showed high positive ERβ staining, and 87 cases (66%) had low positive ERβ staining; only 5 cases (4%) had no nuclear staining. Pancreatic neuroendocrine tumors with small size (P = 0.02), low World Health Organization grade (P = 0.02), and low American Joint Committee on Cancer stage (P = 0.006) more frequently showed high positive ERβ staining. Among the estrogen-induced genes studied, PanNETs had significantly higher expression of PR, EIG121, IGF-1, sFRP1, and sFRP4 compared with normal pancreas, independent of age or sex. High positive ERβ staining was associated with an increased expression of PR (P < 0.001) and EIG121 (P = 0.02).

Conclusions: Our study showed that PanNETs with favorable prognostic features have higher ERβ expression, which is associated with up-regulated PR and EIG121 messenger RNA expression. Estrogen regulation in PanNETs could potentially help in risk stratification and provide a rational target for novel treatment strategies.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Ataxia Telangiectasia Mutated Proteins / biosynthesis
  • Ataxia Telangiectasia Mutated Proteins / genetics
  • Estrogen Receptor alpha / analysis
  • Estrogen Receptor beta / biosynthesis*
  • Estrogen Receptor beta / genetics
  • Estrogens / physiology*
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Insulin-Like Growth Factor I / biosynthesis
  • Insulin-Like Growth Factor I / genetics
  • Ki-67 Antigen / analysis
  • Male
  • Middle Aged
  • Molecular Targeted Therapy*
  • Neoplasm Grading
  • Neoplasm Proteins / biosynthesis*
  • Neoplasm Proteins / genetics
  • Neoplasm Staging
  • Neoplasms, Hormone-Dependent / drug therapy
  • Neoplasms, Hormone-Dependent / genetics
  • Neoplasms, Hormone-Dependent / metabolism*
  • Neuroendocrine Tumors / drug therapy
  • Neuroendocrine Tumors / genetics
  • Neuroendocrine Tumors / metabolism*
  • Pancreatic Neoplasms / drug therapy
  • Pancreatic Neoplasms / genetics
  • Pancreatic Neoplasms / metabolism*
  • Proto-Oncogene Proteins / biosynthesis
  • Proto-Oncogene Proteins / genetics
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • RNA, Neoplasm / biosynthesis
  • RNA, Neoplasm / genetics
  • Receptor, IGF Type 1 / biosynthesis
  • Receptor, IGF Type 1 / genetics
  • Receptors, Estrogen
  • Receptors, Progesterone / biosynthesis
  • Receptors, Progesterone / genetics
  • Tumor Burden
  • Young Adult

Substances

  • Estrogen Receptor alpha
  • Estrogen Receptor beta
  • Estrogens
  • Ki-67 Antigen
  • Neoplasm Proteins
  • Proto-Oncogene Proteins
  • RNA, Messenger
  • RNA, Neoplasm
  • Receptors, Estrogen
  • Receptors, Progesterone
  • SFRP4 protein, human
  • Insulin-Like Growth Factor I
  • Receptor, IGF Type 1
  • ATR protein, human
  • Ataxia Telangiectasia Mutated Proteins