Since colon cancers are heterogeneously differentiated, we set out to determine if the GRPR gene was mutated as a function of tumor cell differentiation in archived human colon cancers.
The levels of GRPR expression in the tumor and adjacent normal epithelium of individual patients with SCCHN were correlated (r =.652; P =.001), suggesting that increased GRPR expression is an early event in SCCHN formation.
Although GRP is known to have a variety of biological functions, only limited information is available concerning expression of proGRP mRNA and protein, and that of the receptor for GRP (GRPR) in SCLC tumors.
RT-PCR analyses revealed that the expression of mRNA for receptors of GRP (GRPR/BRS-1) and Neuromedin B (NMBR/BRS-2) on tumors was significantly decreased in all the treated groups.
Mice administered a control adenoviral vector encoding the gastrin-releasing peptide receptor did not have tumor localization of [(111)In]-DTPA-D-Phe1-octreotide (<1.6% ID/g), demonstrating specificity of [(111)In]-DTPA-D-Phe1-octreotide for the AdCMVhSSTr2 induced tumor cells.
The expression of GRPr in human ovarian cancer cells can be accomplished both in vitro and in vivo by using AdCMVGRPr, with the in vivo tumor localization of [125I]-mIP-bombesin being significantly greater than in control animals.