Bombesin inhibits growth of pancreatic ductal adenocarcinoma (H2T) in nude mice

Antonio Farre, Jin Ishizuka, Guillermo Gomez, B. Mark Evers, Rami Saydjari, Ja Young Koo, Courtney M. Townsend, James C. Thompson

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


Bombesin (BBS), a tetradecapeptide, stimulates growth of various types of cells, including fibroblasts and human small cell lung cancer, and has been termed the universal "on-switch" due to its ability to stimulate the release of numerous hormones. In addition, BBS receptors have been identified in normal and neoplastic pancreatic tissue. A pancreatic ductal adenocarcinoma cell line (H2T), established in our laboratory, possesses specific binding sites for BBS. The purpose of this study was to examine the effect of BBS on the growth of H2T tumors transplanted into athymic nude mice. H2T cells (5 x 106cells/mouse) were injected s.c. into the interscapular region of the nude mice and then the mice were randomized into two groups (n = 10/group). Mice received either 0.1 ml of saline with 0.1% bovine serum albumin (BSA) (control) or 0.1 ml BBS (5 μg/kg) intra-peritoneally, three times/day. Tumor area was measured twice weekly until the mice were killed (day 32), when tumor and normal pancreas were removed, weighed, and assayed for DNA and protein content. Administration of BBS significantly inhibited H2T tumor area, weight, and DNA and protein content. Conversely, growth of normal pancreas, removed as an in vivo bioassay so as to ensure the efficacy of BBS, was stimulated. We conclude that BBS is a growth inhibitory factor for H2T tumors and that different mechanisms may be responsible for the differential growth effects elicited by normal and neoplastic pancreas in response to BBS.

Original languageEnglish (US)
Pages (from-to)652-656
Number of pages5
Issue number5
StatePublished - Sep 1994


  • Bombesin
  • Pancreatic cancer
  • Pancreatic growth

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Hepatology
  • Endocrinology


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