Somatostatin receptor type 2 gene expression in neuroblastoma, measured bycompetitive RT-PCR, is related to patient survival and to somatostatin receptor imaging by indium-111-pentetreotide

Citation
C. Orlando et al., Somatostatin receptor type 2 gene expression in neuroblastoma, measured bycompetitive RT-PCR, is related to patient survival and to somatostatin receptor imaging by indium-111-pentetreotide, MED PED ONC, 36(1), 2001, pp. 224-226
Citations number
10
Categorie Soggetti
Pediatrics
Journal title
MEDICAL AND PEDIATRIC ONCOLOGY
ISSN journal
00981532 → ACNP
Volume
36
Issue
1
Year of publication
2001
Pages
224 - 226
Database
ISI
SICI code
0098-1532(200101)36:1<224:SRT2GE>2.0.ZU;2-Y
Abstract
Background We previously reported that human neuroblastoma cell lines, and primary neuroblastoma tumors expressed a variable amount of mRNA for type 2 somatostatin (sst2) receptor gene. We also found that high level of sst2 e xpression were positively related to patient survival. Procedure. We studie d retrospectively 49 primary neuroblastomas. To detect and measure sst2 mRN A expression we developed a quantitative RT-PCR based on competitive PCR. W hen possible the number of MYCN copies was also measured with competitive P CR. Results. We found that the lowest level of sst2 mRNA was detected in ad vanced stages of neuroblastomas (stage IV) when compared with the other sta ges (P < 0.005). Patients with high levels of sst2 expression (>7 x 10(7) m olecules/mug RNA) had a cumulative survival better than those with low sst2 expression (P < 0.0005). This predictive independent value of sst2 (P = 0. 005) is retained after stratification for N-myc amplification. Finally we v erified that the ex vivo sst2 gene expression in tumor samples was positive ly related (P< 0.01) to the in vivo semiquantitative determination of sst2 protein, assessed by (111)ln-pentetreotide imaging. Conclusions. Our data i ndicate that the measurement of sst2 mRNA measurement could represent a rel evant tool in the prediction of neuroblastoma outcome, independently from M YCN amplification. Med. Pediatr. Oncol. 36:224-226, 2001. (C) 2001 Wiley-Li ss, Inc.