Veterinarska stanica, Vol. 54 No. 6, 2023.
Pregledni rad
https://doi.org/10.46419/vs.54.6.1
Pathophysiology of mast cell tumour in humans and animals
Siniša Faraguna
; Veterinarski fakultet Sveučilišta u Zagrebu, Hrvatska
Romana Turk
; Veterinarski fakultet Sveučilišta u Zagrebu, Hrvatska
Sažetak
This review article investigates the current knowledge of the pathophysiological mechanisms for the formation of mast cell tumours in different animal species and humans. Based on the available literature data, the biological behaviour and forms of mast cell tumour occurring in animals and people were compared, and the essential features of these tumours, such as incidence and the possibility of spread, were examined. The pathogenesis of mast cell tumour formation is not yet fully elucidated though it is assumed to be multifactorial. Breed predisposition to mast cell tumour formation raises the suspicion that pathogenesis is based on a genetic component, where a mutation of the gene that codes the receptor for tyrosine kinase activity on the mast cell membrane for the binding of stem cell factor (SCF) plays an important role. Mutations in the KIT gene causes production of a KIT receptor that is constitutively activated in the absence of a ligand, i.e., stem cell factor (SCF), which leads to mast cell proliferation and development of the mast cell tumour. Mutations in the KIT gene in dogs are commonly located on exon 11, which codes the regulated juxtamembrane domain of the KIT receptor, while in humans with mastocytosis, mutations are commonly found on exon D816V at the 2447 position of coding sequence of the KIT gene. Mutations in the KIT gene in dogs are associated with progression and poor prognosis of the mast cell tumour. In contrast, such mutations are not associated with disease prognosis in cats or humans. However, they play an essential role in diagnosis and therapy in humans.
Ključne riječi
mast cell tumour; KIT mutation; dogs; humans; comparative approach
Hrčak ID:
291183
URI
Datum izdavanja:
19.5.2023.
Posjeta: 418 *