05) [43]. In breast cancer, benign lesions of the breast showed weak CSE1L staining, while 70% – 90% of breast tumor cells were heavily stained for CSE1L [9]. In serous ovarian carcinoma, moderate to strong immunostaining of CSE1L was observed in 34 of 41 cases (83%) of serous carcinomas, and CSE1L immunoreactivity was positively related to the frequency of apoptotic bodies (p = 0.0170),

the tumor grade (p = 0.0107), and adverse outcomes (p = 0.0035) [44]. Peiro et al. reported that CSE1L protein reactivity was present in 100% of 69 ovarian carcinomas, and a significant reciprocal correlation was observed between high levels of CSE1L and the histological type, FIGO (International Federation of Obstetrics and Gynecology) stage III and grade 3, residual tumors of > 2 cm, selleck kinase inhibitor and 20q13.2 (ZNF217 gene) amplification (> four copies in > 20% cells) [45]. A tissue array study composed of 244 serous ovarian tumors of different grades (0-3) and stages (I-IV) showed a higher expression of CSE1L in poorly compared to highly differentiated invasive ovarian tumors [46]. An analysis of 89 endometrial carcinomas and 56 samples of non-neoplastic adjacent endometrium showed that CSE1L was expressed in 93% of endometrial carcinomas

neoplastic tissues, while lower levels of CSE1L expression were observed in the adjacent endometrium compared to the carcinomas (p = 0.003). Also, CSE1L expression was higher in grade 3 tumors (p = 0.002) [22]. Boni et al. studied the expression of CSE1L MRT67307 concentration in 27 control benign and 55 malignant melanocytic lesions (including 32 primary and 23

metastatic lesions), and their results showed that only 13 of the 27 benign melanocytic lesions stained positive for CSE1L [7]. However, 5 of 7 lentigo maligna melanomas, 11 of 12 superficial spreading melanomas, and all acrolentiginous (n = 7) and nodular (n = 6) melanomas showed medium to high intensity immunoreactivity for CSE1L staining [7]. All metastatic melanomas (n = 23) they studied showed strong CSE1L staining [7]. Also, CSE1L detection in check details clinical stages according to the International Union Against Cancer (UICC) showed an increase from 43% ± 34% CSEL-positive cells Epothilone B (EPO906, Patupilone) in stage I, to 53% ± 26% in stage II, 68% ± 24% in stage III, and 72% ± 24% in stage IV [7]. In normal lymphoid tissue and malignant lymphomas, low-grade non-Hodgkin’s lymphoma revealed weak CSE1L staining, with 10% to 60% of all cells positive [6]. In contrast, highly malignant non-Hodgkin’s lymphoma and malignant cells of Hodgkin’s disease displayed very strong CSE1L positivity, with staining of up to 80% of atypical cells [6]. CSE1L was recently shown to be expressed in brain pilocytic astrocytomas [47]. The expression of CSE1L was also reported to be higher in the primary and metastatic human colorectal carcinoma compared to the normal colon mucosa (p < 0.0001) [48].