OBJECTIVE: To determine the frequency of HER2 genetic abnormalities in renal cell carcinoma (RCC) and hence assess the potential suitability of Herceptin immunotherapy. PATIENTS AND METHODS: Tumours from 27 patients with RCC were assessed; all patients had undergone nephrectomy. Benign renal tissue from the nephrectomy specimens was studied in seven patients. Gene amplification was assessed using fluorescent in-situ hybridization, and protein over-expression using immunohistochemistry. RESULTS: Twenty-four patients had clear cell renal carcinoma, two had papillary renal carcinoma and one a sarcomatoid variant carcinoma. There was no HER2 amplification in the tumours or the benign renal tissue. Polysomy 17 was detected in 11 of 27 tumours (41%) and increased HER2 copy number in seven (26%). Both polysomy 17 and increased HER2 copy number were absent in the benign renal tissue. Three tumours (11%) and six of the seven benign renal tissue samples over-expressed the HER2 protein. CONCLUSIONS: HER2 amplification is absent and protein over-expression uncommon in RCC. This casts doubt on the suitability of Herceptin in the treatment of RCC.
OBJECTIVE: To determine the frequency of HER2genetic abnormalities in renal cell carcinoma (RCC) and hence assess the potential suitability of Herceptin immunotherapy. PATIENTS AND METHODS: Tumours from 27 patients with RCC were assessed; all patients had undergone nephrectomy. Benign renal tissue from the nephrectomy specimens was studied in seven patients. Gene amplification was assessed using fluorescent in-situ hybridization, and protein over-expression using immunohistochemistry. RESULTS: Twenty-four patients had clear cell renal carcinoma, two had papillary renal carcinoma and one a sarcomatoid variant carcinoma. There was no HER2 amplification in the tumours or the benign renal tissue. Polysomy 17 was detected in 11 of 27 tumours (41%) and increased HER2 copy number in seven (26%). Both polysomy 17 and increased HER2 copy number were absent in the benign renal tissue. Three tumours (11%) and six of the seven benign renal tissue samples over-expressed the HER2 protein. CONCLUSIONS:HER2 amplification is absent and protein over-expression uncommon in RCC. This casts doubt on the suitability of Herceptin in the treatment of RCC.
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