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In Vitro Modeling of the Clinical Interactions Between Octreotide and ¹¹¹In-Pentetreotide: Is There Evidence of Somatostatin Receptor Downregulation?

¹ Department of Surgery, Louisiana State University Health Sciences Center, New Orleans, Louisiana; ² Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa; and ³ Stanley S. Scott Cancer Center and Veterans Administration Medical Center, New Orleans, Louisiana

Correspondence: For correspondence or reprints contact: Catherine T. Anthony, PhD, Department of Surgery, Louisiana State University Health Sciences Center, 1542 Tulane Ave., New Orleans, LA 70112. E- mail: bombesin1{at}aol.com

Some authors have suggested that chronic octreotide use enhances the efficiency of radiolabeled somatostatin receptor (sst) imaging. Conversely, desensitization of sst on tumor tissue (tachyphylaxis) may occur occasionally in patients on chronic octreotide therapy. Assuming that chronic exposure to octreotide induces tachyphylaxis, we hypothesized that chronic exposure of sst subtype 2 (sst₂)–expressing cells to octreotide would downregulate binding of ¹¹¹In-pentetreotide to sst and that this downregulation would be due to a reduction in the gene copy number for sst₂. Methods: The clinical scenarios of acute (24 h) and chronic (2 wk) octreotide use, followed by either nuclear imaging exposure (8.6 pmol/L) or therapeutic exposure (510 pmol/L) to ¹¹¹In-pentetreotide, were modeled in vitro. Receptor binding in IMR-32 human neuroblastoma cells (high sst₂ expression) and PANC-1 human pancreatic cancer cells (no detectable sst₂ expression) was evaluated. Gene copy numbers for sst subtypes 1–5 in IMR-32 cells were determined by quantitative polymerase chain reaction. Results: Acute or chronic octreotide exposure at low or high doses did not significantly alter sst₂ gene copy numbers or binding of either the diagnostic dose or the therapeutic dose of ¹¹¹In-pentetreotide. Conclusion: In vitro exposure of cells to low or high doses of octreotide for 1–14 d does not result in the development of either tachyphylaxis or upregulation of sst as assessed by changes in gene expression or in high-affinity binding.

Key Words: somatostatin • receptors • gene expression • tachyphylaxis • binding

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