Introduction: Feline mast cell tumours (FeMCTs), overall Accounting for 1e9% of feline neoplasms, are characterized by a highly variable biological behaviour. Frequent post- surgical recurrence, de-novo development of multiple tumours and concurrent visceral and cutaneous involvement justify uncertainty in differentiating benign from malignant forms, with tendency to systemic spread. Materials and Methods: A series of FeMCTs with variable clinical presentation were examined by histology (cell morphology, differentiation, growth pattern, mitotic activity), CD117 immunohistochemistry and c-Kit mutation analysis (exons 8, 9 and 11). Data were correlated with clinical records (clinical signs, TNM stage, haematological abnormalities and 2-year follow-up) to assess their prognostic significance. Results: Twenty cats with 10 solitary cutaneous, five multiple cutaneous and five systemic MCTs were included; nine cats were still alive at the end of the follow-up period. Overall, 29 tumour samples were examined. There were 21 well-differentiated, three pleomorphic and five atypical FeMCTs; mean mitotic activity was 9/10 high power fields. Low to high CD117 expression was observed in 18 cases. Further c-Kit mutations, beside those previously described in FeMCT, were found. Conclusions: This study investigated the effects of c-Kit dysregulation on FeMCT biological behaviour and also potentially allowed the identification of those patients that may benefit from molecular targeted therapies.
Sabattini S, Guadagni-Frizzon M, Turba ME, Gentilini F, Capitani O, Bettini G (2012). KIT receptor dyregulations in feline mast cell tumours and systemic mastocytosis..
KIT receptor dyregulations in feline mast cell tumours and systemic mastocytosis.
SABATTINI, SILVIA;GENTILINI, FABIO;CAPITANI, OMBRETTA;BETTINI, GIULIANO
2012
Abstract
Introduction: Feline mast cell tumours (FeMCTs), overall Accounting for 1e9% of feline neoplasms, are characterized by a highly variable biological behaviour. Frequent post- surgical recurrence, de-novo development of multiple tumours and concurrent visceral and cutaneous involvement justify uncertainty in differentiating benign from malignant forms, with tendency to systemic spread. Materials and Methods: A series of FeMCTs with variable clinical presentation were examined by histology (cell morphology, differentiation, growth pattern, mitotic activity), CD117 immunohistochemistry and c-Kit mutation analysis (exons 8, 9 and 11). Data were correlated with clinical records (clinical signs, TNM stage, haematological abnormalities and 2-year follow-up) to assess their prognostic significance. Results: Twenty cats with 10 solitary cutaneous, five multiple cutaneous and five systemic MCTs were included; nine cats were still alive at the end of the follow-up period. Overall, 29 tumour samples were examined. There were 21 well-differentiated, three pleomorphic and five atypical FeMCTs; mean mitotic activity was 9/10 high power fields. Low to high CD117 expression was observed in 18 cases. Further c-Kit mutations, beside those previously described in FeMCT, were found. Conclusions: This study investigated the effects of c-Kit dysregulation on FeMCT biological behaviour and also potentially allowed the identification of those patients that may benefit from molecular targeted therapies.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.


