KIT is expressed not only in tumors derived from hematopoietic stem cells, melanocytes, germ cells, mast cells, and interstitial cells of Cajal, but also in other malignancies such as chromophobe renal cell carcinoma. This pattern of KIT expression prompted us to investigate the expression and mutation of c-kit gene exons 9, 11, 13, 17, and intron 17 in the different subtypes of renal cell carcinomas (n ¼ 66) and non-neoplastic kidneys (n ¼ 12). We found that KIT showed strong immunoreactivity in the cytoplasm of papillary renal cell carcinomas (100%), but on the cell membranes of chromophobe renal cell carcinomas (100%). Interestingly, a specific point mutation of the c-kit intron 17 (T-4A) was found only in papillary renal cell carcinomas (94%). Our study demonstrates that the expression pattern and one mutation of c-kit may distinguish papillary renal cell carcinomas.

Progenitor cells, termed oval cells, are involved in the pathogenesis of hepatocellular carcinoma (HCC) in animal models. By immunolabeling for c-kit and CD34 in human hepatitis B virus-associated cirrhosis with HCC (50 cases) and those with cirrhosis alone (10 cases), we found c-kit+ tumor cells in tumor tissue in 40 of 50 HCCs. The proportion was less than 0.1% of total tumor cell volume in most HCCs. Immunostaining for c-kit also was detected in sinusoidal endothelial cells in 43 of 50 HCCs. The incidence of oval cell occurrence in the adjacent nonneoplastic tissue in cases of HCC was high (44/50). The occurrence of oval cells, c-kit+ tumor cells, and c-kit+ sinusoidal cells in cases of human hepatitis B virus-associated HCC suggests that oval cell proliferation might be associated with the development of human hepatitis B virus-associated HCC. Furthermore, the c-kit+ sinusoidal cells might have a role in angiogenesis and progression of human hepatitis B virus-associated HCC.

and/or immunohistochemistry for lymphoid cell markers, EBV proteins, and CD21. RESULTSEBER-ISH signals were detected in five of 73 RCC tissues (6.8%), but in none of 18 nonneoplastic kidneys. Interestingly, EBER-ISH was positive only in five of the 10 sarcomatoid RCCs, and of these, four also showed amplification of EBNA-1. EBV was located exclusively in the tumour-infiltrating B lymphocytes of sarcomatoid RCCs. The genotype of EBV was determined as type 1. A few EBV-infected B cells expressed BZLF1 (an EBV immediate-early gene product) while none expressed EBNA-2 or latent membrane protein 1. This indicates that the B cells are of EBV latency type I, often replicating EBV. EBV infection did not affect the survival rates of patients with sarcomatoid RCC ( P = 0.635, Kaplan-Meier analysis, log-rank test). CONCLUSIONEBV is present only in tumour-infiltrating B lymphocytes of sarcomatoid RCCs. The present study suggests that sarcomatoid RCC modulates a function of EBV-specific T cells controlling EBV replication, or stimulates differentiation of memory B cells into plasma cells. KEYWORDS Epstein-Barr virus infections, tumourinfiltrating lymphocytes, renal cell carcinoma OBJECTIVETo determine whether Epstein-Barr virus (EBV) infection is related to renal cell carcinoma (RCC) tissues. MATERIALS AND METHODSWe investigated EBV infection and its genotypes in 73 cases of different types of RCC and 18 of non-neoplastic kidney. EBV infection and its genotypes were determined by EBV-encoded RNAs in situ hybridization (EBER-ISH) and polymerase chain reactions for EBV-encoded nuclear antigen 1 (EBNA-1) and EBNA-3C. The immunophenotype and EBV status of the EBV-infected cells were examined by double-labelling of EBER-ISH

Neurofibromatosis type 1 is characterized by cutaneous neurofibromas and pigmented lesions of the skin called café au lait spots. Although neurofibromatosis type 1 represents a major risk factor for the development of malignancy, especially of nervous system tumors, malignant lymphoma rarely occurs in a patients with neurofibromatosis type 1. Recently, a 77-year-old woman with neurofibromatosis type 1 was diagnosed as non-Hodgkin’s Lymphoma (diffuse large B cell). She had multiple café au lait spots, neurofibromas and right axillary lymph node enlargement. An abdominal CT scan demonstrated a left pelvic mass and para-aortic lymphadenopathy. Because non-Hodgkin’s Lymphoma in a neurofibromatosis patient has never been reported in Korea, herein, we describe this case and include a review of the literature.