KIT (CD117), a tyrosine kinase receptor, has not been widely studied in epithelial tumours. In a systematic immunohistochemical survey of KIT expression on tissue arrays incorporating 671 cases, it was found that thymic carcinomas frequently express KIT. Twenty-two thymic carcinomas, 110 thymomas, and 16 non-neoplastic thymus glands were retrieved for further analyses. Immunohistochemically, 19 (86%) thymic carcinomas revealed heterogeneous to diffuse membranous positivity, whereas no thymomas or normal thymus glands contained positive epithelial cells. Using reverse transcriptase-polymerase chain reaction (RT-PCR), c-kit transcripts could be demonstrated in all immunohistochemically positive cases. PCR amplification and direct sequencing of the c-kit juxtamembrane domains (exons 9 and 11) and tyrosine kinase domain (exons 13 and 17) were also performed on the thymic carcinomas but mutations were not found. Some non-thymic epithelial tumours showed frequent KIT expression including adenoid cystic carcinomas of the salivary gland (100% positive), chromophobe renal cell carcinomas (94%), renal oncocytomas (67%), and neuroendocrine tumours (34%). Other carcinomas were infrequently immunoreactive for KIT. The findings of this study suggest that KIT is involved in the pathogenesis of thymic carcinomas. The overexpression of KIT in thymic carcinomas has potential diagnostic utility in differentiating these tumours from thymomas and carcinomas arising from other sites, which express KIT infrequently.

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Our results showed that HPV16 and betel quid chewing were two major risk factors for OSCC in Taiwan, indicating that they act through different mechanisms in the pathogenesis of OSCC.

Surgical margins prognostically influence survival in both patients undergoing primary surgery and those undergoing reoperation for relapse of extremity STS. In primary surgery, the chance of achieving adequate margin may reflect the underlying aggressiveness of tumors.

KIT expression has not been studied substantially in renal tumors. We analyzed the immunohistochemical expression for KIT in 256 conventional renal cell carcinomas (RCCs), 29 chromophobe RCCs, 25 papillary RCCs, 6 collecting duct RCCs, 6 unclassified RCCs, 7 renal oncocytomas, 20 urothelial carcinomas, 7 nephroblastomas, and 23 angiomyolipomas. We found that 24 chromophobe RCCs (83%) and 5 renal oncocytomas (71%) revealed membranous immunoreactivity for KIT while none of the RCCs of other types expressed KIT immunohistochemically. Sporadic cases of urothelial carcinoma and nephroblastoma were focally positive for KIT. All angiomyolipomas were negative. Genomic DNA extracted from the chromophobe RCCs and renal oncocytomas was submitted for polymerase chain reaction and direct sequencing of the juxtamembrane (exons 9 and 11) and tyrosine kinase (exons 13 and 17) domains. No mutation was found. Our results demonstrate that KIT could be a useful immunophenotypic marker for chromophobe RCC and renal oncocytoma; therefore, it has value for the precise classification of renal cortical epithelial tumors. However, the therapeutic relevance of KIT overexpression in these tumors is uncertain owing to the lack of mutations that would lead to constitutive activation of the protein.