Knock-in murine models of familial gastrointestinal stromal tumours

In recent years, gastrointestinal stromal tumour (GIST) has emerged from a poorly understood group of mesenchymal tumours to a distinct pathological entity that has become a leading model for new therapies targeting kinases. GIST pathogenesis is driven by receptor tyrosine kinase-activating mutation...

Full description

Saved in:
Bibliographic Details
Published in:The Journal of pathology 2008-03, Vol.214 (4), p.407-409
Main Author: Gunawan, B
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Disease Models, Animal
Gastroenterology. Liver. Pancreas. Abdomen
Gastrointestinal Stromal Tumors - genetics
gastrointestinal stromal tumour (GIST)
Germ-Line Mutation
germline mutation
Humans
interstitial cell of Cajal
Investigative techniques, diagnostic techniques (general aspects)
KIT gene
knock-in strategy
Medical sciences
Mice
Mice, Mutant Strains
mouse model
Neoplastic Syndromes, Hereditary - genetics
Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques
Proto-Oncogene Proteins c-kit - genetics
Signal Transduction - genetics
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
Tumors
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:In recent years, gastrointestinal stromal tumour (GIST) has emerged from a poorly understood group of mesenchymal tumours to a distinct pathological entity that has become a leading model for new therapies targeting kinases. GIST pathogenesis is driven by receptor tyrosine kinase-activating mutations most often in KIT or PDGFRA that may be sporadic or result in familial GIST syndromes. In a recent issue of The Journal of Pathology (J Pathol 2008;214:302-311), Nakai and colleagues report that mutation of the previously un-modelled tyrosine kinase II domain of KIT generates a spectrum of features very similar to that in two human GIST families. Knock-in mouse models of GIST may prove extremely useful in pre-clinical evaluation of kinase-targeted compounds and of the mechanism of drug resistance, but intriguingly it now seems clearer that the distribution of GIST in mouse models and humans is different. Copyright © 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
ISSN:0022-3417
1096-9896
DOI:10.1002/path.2315