| First Author | Gunawan B | Year | 2008 |
| Journal | J Pathol | Volume | 214 |
| Issue | 4 | Pages | 407-9 |
| PubMed ID | 18200631 | Mgi Jnum | J:131823 |
| Mgi Id | MGI:3774691 | Doi | 10.1002/path.2315 |
| Citation | Gunawan B (2008) Knock-in murine models of familial gastrointestinal stromal tumours. J Pathol 214(4):407-9 |
| abstractText | 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 (c) 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. |
