Rabbit Anti-Human KRT18 Polyclonal antibody

Wilms' tumours (WT) and adult papillary renal cell tumours (pRCT) are associated with precursor lesions of embryonic origin. The aim of this study was to analyse the expression of WT1, KRT7, KRT8, KRT18 and KRT19 genes by immunohistochemistry in 74 precursor lesions associated with WTs, pRCTs and mucinous tubular and spindle cell carcinomas (MTSCC). All precursor lesions associated with Wilms' tumours were positive for WT1, whereas all precursor lesions in pRCT and MTSCC-bearing kidneys were negative. None of the WT-associated lesions were positive for KRT7, but 69-80% of lesions associated with pRCTs and MTSCCs were positive for KRT7. KRT8, KRT18 and KRT19 were found to be expressed in 80-100% of all types of precursor lesions. Our findings indicate that the precursor lesions analysed in this study are committed in an early stage of cellular differentiation to the development of either Wilms' tumours or papillary RCTs and MTSCCs.

To understand the molecular alterations driving the progression of ductal carcinoma in situ (DCIS), we compared patients with pure DCIS and patients with DCIS and synchronous invasive breast cancer (IBC). Twelve patients with extensive pure DCIS were included as a representation of indolent lesions with Limited invasive capacity. These cases were matched with 12 patients with a Limited DCIS component and IBC, representing lesions with a high invasive potential. Matching included age and surrogate DCIS subtypes. Gene expression profiling was performed on DCIS cells to identify transcriptional differences between these two groups. The identified genes were validated by immunohistochemistry. Nine genes showed significantly different expression. Most of these genes were highly expressed in DCIS samples with IBC, including PLAU (P = 0.002), COL1A1 (P = 0.006), KRT81 (P = 0.009), S100A7 (P = 0.015), SCGB1D2 (P = 0.023), KRT18 (P = 0.029), and NOTCH3 (P = 0.044), whereas EGFR and CXCL14 showed a higher expression in cases with pure DCIS (P = 0.015 and P = 0.028, respectively). This difference was only significant for SCGB1D2 (P = 0.009). Hierarchical clustering revealed distinct clustering of patients with and without invasion. Patients with pure DCIS have a different gene expression pattern as compared to patients with DCIS and synchronous IBC. These genes may pinpoint to driver pathway(s) that play an important role in DCIS progression.