Absence or low IGF-1R-expression in esophageal adenocarcinoma is associated with tumor invasiveness and radicality of surgical resection

Kirstin Bruijn, Katharina Biermann, J (Joël) Shapiro, Fadime Dogan - Oruç, Manon Spaander, J.A.M.J.L. Janssen, Bas Wijnhoven, Gerard Borsboom, Leo Hofland, Casper van Eijck

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Abstract

Background and ObjectivesEsophageal adenocarcinoma (EAC) incidence increases, maybe due to increasing prevalences of obesity and diabetes. Concurrent hyperinsulinemia might promote carcinogenesis via the insulin-like growth factor-I receptor (IGF-1R). Expression of the IGF-1R was studied in correlation with diabetes and prognostic parameters. MethodsPatients with EAC undergoing esophagectomy were prospectively selected. From resected tumors a tissue microarray was constructed. Immunohistochemistry evaluated IGF-1R-expression. Logistic-, cox regression models and survival analyses assessed if diabetes and IGF-1R-expression were associated with prognostic parameters. IGF-1R-expression in normal and Barrett tissues was studied. ResultsAbsence or low IGF-1R-expression was associated with T3-, grade 3 tumors and R1 resections (P=0.001, P=0.025, P<0.001, respectively). Logistic regression showed that this was associated with R1 resections (HR 0.24, 95%CI 0.11-0.52). Diabetes was not associated with IGF-1R-expression (P=0.612). Absence or low IGF-1R-expression decreased 5-year overall survival (P=0.023) univariably, but not multivariably. IGF-1R-expression was present in Barrett tissues, but diminished in high-grade dysplasia. ConclusionsAbsence or low expression of IGF-1R was associated with high grade- and advanced tumors and less radical resections. IGF-1R might be a tumor marker in Barrett's esophagus since a change in expression patterns was found in the course from normal esophageal tissue to adenocarcinoma. J. Surg. Oncol. 2015 111:1047-1053. (c) 2015 Wiley Periodicals, Inc.
Original languageUndefined/Unknown
Pages (from-to)1047-1053
Number of pages7
JournalJournal of Surgical Oncology
Volume111
Issue number8
DOIs
Publication statusPublished - 2015

Research programs

  • EMC MM-01-39-01
  • EMC MM-03-24-01
  • EMC MM-03-47-02-A
  • EMC MM-04-20-01
  • EMC MM-04-47-07
  • EMC NIHES-02-65-01

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