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Gastrointestinal stromal tumour lacking mutations in the KIT and PDGFRA genes in a cat
Y Fujii1,2, R Iwasaki2, S Ikeda3
1Joint Graduate School of Veterinary Sciences, Gifu University, Gifu, Gifu, Japan.
Abstract:
Molecular subtyping in gastrointestinal stromal tumours is a useful method for predicting the efficacy of treatment using tyrosine kinase inhibitors in humans. However, owing to the paucity of reports on mutational analyses, the association between genetic mutations and the therapeutic response to tyrosine kinase inhibitors remains unclear in feline gastrointestinal stromal tumours. In this report, we describe the case of a cat with a gastrointestinal stromal tumour which was unresponsive to tyrosine kinase inhibitors. A mutational analysis revealed that the cat lacked mutations in both the KIT and platelet-derived growth factor receptor-alpha (PDGFRA) genes. Our findings are consistent with the fact that KIT/PDGFRA wild-type gastrointestinal stromal tumours are less responsive to tyrosine kinase inhibitors in humans. This signifies the need for further evaluation and possibly individualised treatment for gastrointestinal stromal tumours in cats on the basis of mutational analyses.
Insights
Molecular subtyping of feline gastrointestinal stromal tumors (GISTs) is crucial. This study found a GIST lacking KIT/PDGFRA mutations was unresponsive to tyrosine kinase inhibitors, suggesting a need for genetic analysis in feline GIST treatment.
Area of Science:
- Veterinary Oncology
- Molecular Pathology
- Comparative Oncology
Background:
- Molecular subtyping of gastrointestinal stromal tumors (GISTs) aids in predicting treatment response to tyrosine kinase inhibitors (TKIs) in humans.
- Limited data exists on the genetic mutations in feline GISTs and their association with TKI efficacy.
Observation:
- A case of feline GIST was identified that was unresponsive to TKI therapy.
- Mutational analysis of the feline GIST revealed wild-type status for both KIT and PDGFRA genes.
Findings:
- Feline GIST lacking KIT/PDGFRA mutations exhibit resistance to TKIs, mirroring observations in human GIST.
- The absence of specific genetic mutations correlates with a lack of therapeutic response to targeted therapies.
Implications:
- Genetic mutational analysis is essential for guiding individualized TKI treatment strategies in feline GIST.
- Further research is needed to understand the molecular basis of TKI resistance in feline GIST.
- Comparative oncology studies can inform veterinary and human GIST treatment paradigms.
