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Co expression of SCF and KIT in gastrointestinal stromal tumours (GISTs) suggests an autocrine/paracrine mechanism

Theou-Anton, N ; Tabone, S ; Brouty-Boye, D ; Saffroy, R ; Rönnstrand, Lars LU ; Lemoine, A and Emile, JF (2006) In British Journal of Cancer 94(8). p.1180-1185
Abstract
KIT is a tyrosine kinase receptor expressed by several tumours, which has for specific ligand the stem cell factor (SCF). KIT is the main oncogene in gastrointestinal stromal tumours (GISTs), and gain-of-function KIT mutations are present in 70% of these tumours. The aim of the study was to measure and investigate the mechanisms of KIT activation in 80 KIT-positive GIST patients. KIT activation was quantified by detecting phosphotyrosine residues in Western blotting. SCF production was determined by reverse transcriptase PCR, ELISA and/or immunohistochemistry. Primary cultures established from three GISTs were also analysed. The results show that KIT activation was detected in all cases, even in absence of KIT mutations. The fraction of... (More)
KIT is a tyrosine kinase receptor expressed by several tumours, which has for specific ligand the stem cell factor (SCF). KIT is the main oncogene in gastrointestinal stromal tumours (GISTs), and gain-of-function KIT mutations are present in 70% of these tumours. The aim of the study was to measure and investigate the mechanisms of KIT activation in 80 KIT-positive GIST patients. KIT activation was quantified by detecting phosphotyrosine residues in Western blotting. SCF production was determined by reverse transcriptase PCR, ELISA and/or immunohistochemistry. Primary cultures established from three GISTs were also analysed. The results show that KIT activation was detected in all cases, even in absence of KIT mutations. The fraction of activated KIT was not correlated with the mutational status of GISTs. Membrane and soluble isoforms of SCF mRNA were present in all GISTs analysed. Additionally, SCF was also detected in up to 93% of GISTs, and seen to be present within GIST cells. Likewise, the two SCF mRNA isoforms were found to be expressed in GIST-derived primary cultures. Thus, KIT activation in GISTs may in part result from the presence of SCF within the tumours. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
autocrine loop, gastrointestinal tumour, sarcoma, SCF
in
British Journal of Cancer
volume
94
issue
8
pages
1180 - 1185
publisher
Nature Publishing Group
external identifiers
  • pmid:16570044
  • wos:000236910300014
  • scopus:33646123102
  • pmid:16570044
ISSN
1532-1827
DOI
10.1038/sj.bjc.6603063
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Experimental Clinical Chemistry (013016010)
id
390e1a74-29f2-4983-82da-93dfadfda721 (old id 411232)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=%2016570044%20opt=Abstract
date added to LUP
2016-04-01 12:20:53
date last changed
2020-01-12 09:40:21
@article{390e1a74-29f2-4983-82da-93dfadfda721,
  abstract     = {KIT is a tyrosine kinase receptor expressed by several tumours, which has for specific ligand the stem cell factor (SCF). KIT is the main oncogene in gastrointestinal stromal tumours (GISTs), and gain-of-function KIT mutations are present in 70% of these tumours. The aim of the study was to measure and investigate the mechanisms of KIT activation in 80 KIT-positive GIST patients. KIT activation was quantified by detecting phosphotyrosine residues in Western blotting. SCF production was determined by reverse transcriptase PCR, ELISA and/or immunohistochemistry. Primary cultures established from three GISTs were also analysed. The results show that KIT activation was detected in all cases, even in absence of KIT mutations. The fraction of activated KIT was not correlated with the mutational status of GISTs. Membrane and soluble isoforms of SCF mRNA were present in all GISTs analysed. Additionally, SCF was also detected in up to 93% of GISTs, and seen to be present within GIST cells. Likewise, the two SCF mRNA isoforms were found to be expressed in GIST-derived primary cultures. Thus, KIT activation in GISTs may in part result from the presence of SCF within the tumours.},
  author       = {Theou-Anton, N and Tabone, S and Brouty-Boye, D and Saffroy, R and Rönnstrand, Lars and Lemoine, A and Emile, JF},
  issn         = {1532-1827},
  language     = {eng},
  number       = {8},
  pages        = {1180--1185},
  publisher    = {Nature Publishing Group},
  series       = {British Journal of Cancer},
  title        = {Co expression of SCF and KIT in gastrointestinal stromal tumours (GISTs) suggests an autocrine/paracrine mechanism},
  url          = {http://dx.doi.org/10.1038/sj.bjc.6603063},
  doi          = {10.1038/sj.bjc.6603063},
  volume       = {94},
  year         = {2006},
}