Impact of QTc prolongation on the occurrence of adverse events in HCM patients.

<p>Sensitivity, specificity, PPV (positive predictive value), NPV (negative predictive value) and OR (odds ratio; adjusted for age and sex) with 95%-CI (confidence intervals) are given in the table below. AE = adverse events (syncope, presyncope, VT).</p

Influence of disease related factors and medication on the orthostatic test result in 69 HCM patients older than or equal to 40 years.

<p>Values are given as total number of patients (n) or as mean ± SD.</p><p>Influence of disease related factors and medication on the orthostatic test result in 69 HCM patients older than or equal to 40 years.</p

Impact of orthostatic test on the occurrence of adverse events in HCM patients for all patients (A) and for the subgroup of patients > 40 yrs (B).

<p>Sensitivity, specificity, PPV (positive predictive value), NPV (negative predictive value) and OR (odds ratio; adjusted for age and sex) with 95%-CI (confidence intervals) are given in the table below. AE = adverse events (syncope, presyncope, VT).</p

Relationship between orthostatic test result and QTc prolongation.

<p>The percentages of patients with a positive and negative orthostatic test result are given for the group with and without QTc prolongation.</p

Influence of disease related factors and medication on the QTc interval in 100 HCM patients.

<p>Values are given as total number of patients (n) or as mean ± SD.</p><p>Influence of disease related factors and medication on the QTc interval in 100 HCM patients.</p

Patient characteristics by treatment group and standardized differences.

<p>Patient characteristics by treatment group and standardized differences.</p

Univariate associations between baseline characteristics and competing causes of death.

<p>Univariate associations between baseline characteristics and competing causes of death.</p

Results after propensity scoring using the potential confounders age, resection status, ECOG, number of affected nodes, type of vulva surgery and groin dissection.

<p>Results after propensity scoring using the potential confounders age, resection status, ECOG, number of affected nodes, type of vulva surgery and groin dissection.</p

Standardized differences to identify imbalances between treatment groups before and after imputing and inverse-probability-of-treatment-weighting.

<p>Standardized differences to identify imbalances between treatment groups before and after imputing and inverse-probability-of-treatment-weighting.</p

Knockdown of L1CAM significantly reduces metastasis in a xenograft model of human melanoma: L1CAM is a potential target for anti-melanoma therapy

<div><p>Finding additional functional targets for combination therapy could improve the outcome for melanoma patients. In a spontaneous metastasis xenograft model of human melanoma a shRNA mediated knockdown of L1CAM more than sevenfold reduced the number of lung metastases after the induction of subcutaneous tumors for two human melanoma cell lines (MeWo, MV3). Whole genome expression arrays of the initially L1CAM high MeWo subcutaneous tumors revealed unchanged or downregulated genes involved in epithelial to mesenchymal transition (EMT) except an upregulation of Jagged 1, indicating a compensatory change in Notch signaling especially as Jagged 1 expression showed an increase in MeWo L1CAM metastases and Jagged 1 was expressed in metastases of the initially L1CAM low MV3 cells as well. Expression of 17 genes showed concordant regulation for L1CAM knockdown tumors of both cell lines. The changes in gene expression indicated changes in the EMT network of the melanoma cells and an increase in p53/p21 and p38 activity contributing to the reduced metastatic potential of the L1CAM knockdowns. Taken together, these data make L1CAM a highly interesting therapeutic target to prevent further metastatic spread in melanoma patients.</p></div