Ratins (CK), vimentin, epithelial membrane antigen (EMA), CD10 and parvalbumin can be potentially helpful in diagnosis of different subtypes of RCC. Vimentin was reported positive in 0-21 of ChRCC, CD10 in 0-33 of ChRCC, CK7 in 60-100 of ChRCC, CK8 in 50 of ChRCC, CK18 in 100 of ChRCC, CK19 in 33 of ChRCC, CK20 in 12.5 of ChRCC, EMA 75-100 of ChRCC and parvalbumin 100 PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27693494 of ChRCC. Sometimes ChRCC can be mistaken for renal oncocytoma [10,11] (Table 1).Clinical and Histomorphological FeaturesPrognosis in ChRCC is better than in other types of RCC. Five- and 10-year DFS for chromophobe RCC was 83.9Page 2 of(page number not for citation purposes)Journal of Experimental Clinical Cancer Research 2009, 28:http://www.jeccr.com/content/28/1/Table 1: Expression of immunohistological markers of ChRCCImmunohistological markers of ChRCCCK 7 60-CK 8CK 18CK 19CK 20 12.VimentinEMACDParvalbuminPositive APTO-253 web reactivity ( )0-75-0-and 77.9 , respectively [12]. The median time from nephrectomy to metastasis detection, and from metastasis detection to death were twice as long for ChRCC than for other subtypes of RCC (papillary, clear cell RCC) [7]. In univariate analysis: sarcomatoid change (p < 0.001), microscopic necrosis (p = 0.019), tumor size (p = 0.025), pT stage (3.4 vs. 1.2; p = < 0.001), broad alveolar growth (p = 0.012), vascular invasion (p = 0.020), and Fuhrman nuclear grade (grade 4 vs.3 vs 2; p < 0.001) were associated with aggressive ChRCC behavior. Independent predictors (Multivariable Cox Regression) of aggressive ChRCC included: pT stage (pT 3.4 vs. pT 1.2; p = 0.025, relative hazard 3.4), sarcomatoid change (p = 0.013, relative hazard 4.7) and microscopic necrosis (p = 0.020, relative hazard 3.5) [6]. Other factors like: age, sex, histologic subtyping by clear, eosinophilic or mixed cell types, tubulocystic pattern, degenerate or symplastic atypia were not predictors of chromophobe RCC behavior. The patients with aggressive phenotype of chromophobe RCC may be candidates for adjuvant therapies as they become available [6]. ChRCCs are hyperechogenic in ultrasound examination, CT imaging or MRI demonstrate homogeneous enhancement. A spoke-wheel pattern of contrast enhancement is characteristic for ChRCC and for onkocytoma [13]. Most of ChRCCs are sporadic, but sometimes they are associated with BHD (Birt-Hogg-Dub? syndrome [14].cell types. It regulates apoptosis, cell differentiation, proliferation, chemotaxis, and adhesion. Pathologic activation of KIT through gain-of-function mutations leads to neoplasia of KIT-dependent and KIT-positive cell types in different systems: Cajal cells - gastrointestinal stromal tumors (GISTs), myeloid cells - myeloid leukemia. In addition, many tumors have positive KIT immunoreactivity: small cells carcinomas, adenoid cystic carcinoma, chromophobe, thymic and sometimes ovarian and breast carcinomas [18]. In normal tissue of kidney KIT showed weak immunoreactivity only in the cytoplasm of distal tubules [19]. From all RCCs, KIT gene product was detected (overexpression) in membrane of cells ChRCC (88-100 ) [19,20]. This is in agreement with histogenetic origin of chromophobe RCC from distal tubules. KIT expression in classic variant is more often than eosinophilic variant (82 vs. 67 ) [21]. Thus, immunohistochemical detection of KIT expression appears to be useful in diagnosis and treatment of ChRCC. Yamazaki et al. reported upregulation of c-kit gene expression in ChRCCs. The mechanism for the overexpressi.