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Updated: Aug 17, 2026

The Use of Reverse Phase Protein Arrays (RPPA) to Explore Protein Expression Variation within Individual Renal Cell Cancers
Published on: January 22, 2013
Expression of KIT (CD117) in renal cell carcinoma and renal oncocytoma
Stefan Krüger1, Karl Sotlar, Ingo Kausch
1Institute of Pathology, University of Schleswig-Holstein, Campus Lübeck, Lübeck, Germany. krueger@patho.uni-luebeck.de
Objective:
Overexpression of KIT (CD117), a tyrosine kinase receptor, has been reported in a variety of tumors, some of which are susceptible to therapy with imatinib mesylate. Our aim was to analyze KIT expression immunohistochemically in renal cell carcinomas (RCCs) and in oncocytomas.
Methods:
Routinely processed, paraffin-embedded specimens from 61 RCCs and 13 renal oncocytomas were investigated immunohistochemically. Cytoplasmic and membrane-bound KIT staining of tumor cells was determined semiquantitatively. A subset of cases was additionally analyzed for point mutations of c-kit exon 17 by peptide nucleic acid-mediated nested polymerase chain reaction-clamping.
Results:
All cases of oncocytomas and chromophobe RCCs showed membrane-bound KIT positivity, while about three-quarters of cases showed cytoplasmic reactivity. All other types of RCC were found KIT negative. Within the group of chromophobe RCCs, negative cytoplasmatic KIT reactivity was significantly correlated with advanced tumor stage (pT > or = 2; p = 0.036). Analysis of c-kit exon 17 revealed no 'gain-of-function' mutation like the codon 816 Asp-->Val mutation (D816V).
Conclusions:
KIT expression is a hallmark of oncocytoma and chromophobe RCC. Since all other types of RCC were found to be KIT negative, immunohistochemical KIT reactivity may be used as an additional diagnostic criterion to distinguish chromophobe RCC from other RCC types. KIT reactivity and the absence of c-kit mutation D816V in chromophobe RCC justify speculations that imatinib mesylate therapy could be effective in patients with advanced disease.
Insights
KIT (CD117) expression is a key marker for oncocytomas and chromophobe renal cell carcinomas (RCCs). This finding aids in distinguishing chromophobe RCC from other RCC types, potentially guiding imatinib mesylate therapy.
Area of Science:
- Oncology
- Molecular Pathology
Background:
- KIT (CD117) is a tyrosine kinase receptor overexpressed in various tumors.
- Some KIT-expressing tumors respond to imatinib mesylate therapy.
Purpose of the Study:
- To investigate KIT expression in renal cell carcinomas (RCCs) and oncocytomas using immunohistochemistry.
- To assess the diagnostic utility of KIT expression in differentiating RCC subtypes.
Main Methods:
- Immunohistochemical analysis of KIT expression in 61 RCCs and 13 oncocytomas.
- Semiquantitative assessment of cytoplasmic and membrane-bound KIT staining.
- Analysis of c-kit exon 17 for mutations in a subset of cases.
Main Results:
- Oncocytomas and chromophobe RCCs consistently showed membrane-bound KIT positivity.
- Other RCC types were predominantly KIT negative.
- No 'gain-of-function' c-kit mutations, such as D816V, were detected.
Conclusions:
- KIT expression is a characteristic feature of oncocytoma and chromophobe RCC.
- Immunohistochemical KIT analysis can help differentiate chromophobe RCC from other RCC subtypes.
- KIT expression in chromophobe RCC, without specific c-kit mutations, suggests potential efficacy of imatinib mesylate therapy in advanced cases.
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