Pancreatic cancer is the eighth most common cancer and has an overall 5-year survival rate lower than 10%. Because of their ability to regulate gene expression, microRNAs can act as oncogenes or tumor-suppressor genes and so have garnered interest as possible prognostic and therapeutic markers during the last decade. However, the prognostic value of microRNA expression in pancreatic cancer has not been thoroughly investigated. We measured the levels of miR-155, miR-203, miR-210, miR-216, miR-217 and miR-222 by quantitative RT-PCR in a cohort of 56 microdissected pancreatic ductal adenocarcinomas (PDAC). These microRNAs were chosen as they had previously been shown to be differentially expressed in pancreatic tumors compared to normal tissues. The possible association of microRNA expression and patients' survival was examined using multivariate Cox's regression hazard analyses. Interestingly, significant correlations between elevated microRNA expression and overall survival were observed for miR-155 (RR 5 2.50; p 5 0.005), miR-203 (RR 5 2.21; p 5 0.017), miR-210 (RR 5 2.48; p 5 0.005) and miR-222 (RR 5 2.05; p 5 0.035). Furthermore, tumors from patients demonstrating elevated expression levels of all 4 microRNAs possessed a 6.2-fold increased risk of tumor-related death compared to patients whose tumors showed a lower expression of these microRNAs. This study provides the first evidence for an oncogenic activity of miR-155, miR-203, miR-210 and miR-222 in the development of pancreatic cancer as has been reported for other tumor types. Furthermore, the putative target genes for these microRNAs suggest a complex signaling network that can affect PDAC tumorigenesis and tumor progression.Because of its poor prognosis, pancreatic cancer is one of the leading causes of cancer-related death, despite its relative low incidence with 9 cases per 100,000 people. 1 The poor prognosis of patients is a result of the late clinical presentation and the high metastatic potential. Three-fourths of pancreatic carcinomas are ductal adenocarcinomas (PDAC). 2 There are molecular prognostic markers known for pancreatic cancers. For example, higher levels of protein expression of VEGF or EGFR have been shown to associate with poorer survival rates. 3 Besides non-physiological KRAS activation, which is mutated in about 95% of all pancreatic carcinomas, 4 inactivation of known tumor-suppressor genes such as p53 or SMAD4 (deleted in 75% or 55% of all PDACs, respectively) have been demonstrated. 5,6 MicroRNAs are small, non-coding RNAs of endogenous origin, which mainly function as negative regulators of gene expression. The association of altered microRNA expression with cancerogenesis as well as tumor progression is well established. [7][8][9] There is a growing number of microRNAs, which are classified as oncogenes or tumor-suppressor genes. 10 For instance, miR-17-92-cluster has gained interest by being regulated via c-myc and its ability to accelerate tumor formation. 11,12 Also, let-7 expression was described to correlate with a poo...

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Tumor-associated immune cells have been discussed as an essential factor for the prediction of the outcome of tumor patients. Lymphocyte-specific genes are associated with a favorable prognosis in colorectal cancer but with poor survival in renal cell carcinoma (RCC). Flow cytometric analyses combined with immunohistochemistry were performed to study the phenotypic profiles of tumor infiltrating lymphocytes (TIL) and the frequency of T cells and macrophages in RCC lesions. Data were correlated with clinicopathological parameters and survival of patients. Comparing oncocytoma and clear cell (cc)RCC, T cell numbers as well as activation-associated T cell markers were higher in ccRCC, whereas the frequency of NK cells was higher in oncocytoma. An intratumoral increase of T cell numbers was found with higher tumor grades (G1:G2:G3/4 D 1:3:4). Tumor-associated macrophages slightly increased with dedifferentiation, although the macrophage-to-T cell ratio was highest in G1 tumor lesions. A high expression of CD57 was found in T cells of early tumor grades, whereas T cells in dedifferentiated RCC lesions expressed higher levels of CD69 and CTLA4. TIL composition did not differ between older (>70 y) and younger (<58 y) patients. Enhanced patients' survival was associated with a higher percentage of tumor infiltrating NK cells and Th1 markers, e.g. HLA-DRC and CXCR3C T cells, whereas a high number of T cells, especially with high CD69 expression correlated with a worse prognosis of patients. Our results suggest that immunomonitoring of RCC patients might represent a useful tool for the prediction of the outcome of RCC patients.

The aims of this study were, first, to report normative values for jaw movements in Caucasian children and adolescents (maximum opening, laterotrusion, and protrusion) and, second, to investigate the influence of age, gender, and temporomandibular disorders (TMD) on jaw movement capacity. The population-based study included 1,011 randomly selected German children and adolescents, aged 10-17 yr. Case histories, as well as mandibular movements and the presence of TMD, were assessed according to the Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD). The mean +/- standard deviation for maximum opening was 50.6 +/- 6.4 mm, for laterotrusion to the right was 10.2 +/- 2.2 mm, for laterotrusion to the left was 10.6 +/- 2.3 mm, and for protrusion was 8.2 +/- 2.5 mm. Bivariable (t-test) and multivariable (linear regression) analyses showed that normative values for jaw opening capacity were influenced by age and gender. No influence on jaw movement capacity was seen when TMD were present. Based on the distribution of the measurements in the population (lowest decentile), the mandibular mobility of subjects with a maximum opening of < 43 mm and laterotrusive movements < 8 mm or protrusive movements < 5 mm might be considered as being limited. However, these limitations do not necessarily require treatment.

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