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Vol. 89, No. 1-2, 2000
Issue release date: 2000
Section title: Paper
Cytogenet Cell Genet 89:62–66 (2000)
(DOI:10.1159/000015566)

Fine mapping of the human preprocortistatin gene (CORT) to neuroblastoma consensus deletion region 1p36.3→p36.2, but absence of mutations in primary tumors

Ejeskär K.a · Abel F.a · Sjöberg R.-M.a · Bäckström J.b · Kogner P.b · Martinsson T.a
aDepartment of Clinical Genetics, Gothenburg University, Sahlgrenska University Hospital/East, Gothenburg, and bChildhood Cancer Research Unit, Karolinska Institutet, Karolinska Hospital, Stockholm (Sweden)

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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 6/26/2000
Issue release date: 2000

Number of Print Pages: 5
Number of Figures: 2
Number of Tables: 1

ISSN: 1424-8581 (Print)
eISSN: 1424-859X (Online)

For additional information: http://www.karger.com/CGR

Abstract

Abstract.

The processed product of the human gene preprocortistatin, the peptide cortistatin-17 (hCST-17), bears a strong structural resemblance to the peptide somatostatin (SST), which has an identical receptor binding domain. CST has affinity to all known SST receptor (SSTR) subtypes. Expression of both SST and its receptors has been shown in previous studies to have biological and clinical significance in neuroblastomas, with a putative role in tumor differentiation and apoptosis in vivo. In this work we have employed radiation hybrid mapping and BAC physical mapping to map the human preprocortistatin gene (CORT) to chromosome region 1p36.3→p36.2, close to the genetic marker D1S244. D1S244 defines the centromeric border of the smallest region of overlap of deletion in our primary neuroblastoma material. We have also defined the genomic sequence of the gene by BAC sequencing and found that preprocortistatin consists of two exons divided by a 1-kb intron. Two polymorphic sites, neither of which causes amino acid exchange, have been detected in the coding region of the gene. Expression studies showed that preprocortistatin is expressed in neuroblastomas of all different stages, as well as in ganglioneuromas. Through genomic sequencing we made mutation analyses of exonic sequences in 49 primary neuroblastomas of all different stages, but no mutations could be detected.   

© 2000 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: 6/26/2000
Issue release date: 2000

Number of Print Pages: 5
Number of Figures: 2
Number of Tables: 1

ISSN: 1424-8581 (Print)
eISSN: 1424-859X (Online)

For additional information: http://www.karger.com/CGR


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