Correlation of serum levels of miR-625* with the histological type of carcinoma and smoking behavior.

<p>The box plots show the different, relative amounts of miR-625* in healthy controls with unknown smoking behavior (H, n = 30) and all NSCLC patients with ADC (n = 39), SQCLC (n = 35), LCLC (n = 12), and non-smoking (NS, n = 7) and smoking (S, n = 28) behavior (A), in smoking NSCLC patients (S, n = 28) with ADC (n = 12), SQCLC (n = 10) and LCLC (n = 6) (B), and in healthy controls (H, n = 30), NS (n = 7) and S (n = 28) with malignant lung tumors (mal.), NS (n = 9) and S (n = 11) with benign lung tumors (ben.), NS (n = 16) and S (n = 39) with malignant or benign lung tumors (mal.+ben.) (C). As determined by Mann and Whitney-U test, the significant p values of the statistical evaluations of serum RNA and miR levels are indicated above the blots.</p

Evaluation of the diagnostic relevance of levels of total RNA and miRs in serum of healthy individuals, patients with benign lung disease and NSCLC patients.

<p>The box plots show the different, relative amounts of total RNA (A), miR-361-3p (B) and miR-625* (C) which circulate in blood of healthy individuals (n = 30), patients with benign lung disease (n = 20) and NSCLC patients (n = 97). The relative transcript levels of miRs were determined by the low cycle threshold (Ct) values. As determined by Mann and Whitney-U test, the significant p values of the statistical evaluations of serum RNA and miR levels are indicated. The ROC analysis shows the profile of sensitivity and specificity of miR-361-3p and miR-625* concentrations to discriminate NSCLC patients from patients with benign disease and healthy individuals (D). The AUC values and confidence intervals are indicated.</p

Patients' characteristics and correlation of serum RNA and relative levels of circulating miRs with clinical and histopathological parameters of the validation cohort.

α<p>p = 0.048,</p>β<p>p = 0.014,</p>ε<p>p = 0.030,</p>δ<p>p = 0.031;</p>£<p>M0, patients with localized NSCLC;</p>$<p>M1, patients with metastatic NSCLC;</p>#<p>M0 patients;</p><p>p values as determined by Mann Whitney-U test.</p

Differentially regulated microRNAs in healthy individuals versus patients with NSCLC.

<p>Differentially regulated microRNAs in healthy individuals versus patients with NSCLC.</p

MiR profiling by a blood-based microarray.

<p>Hierarchical cluster heat map of miR microarray was performed using microfluid biochips containing 1158 different miRs with serum of 21 NSCLC patients and 11 healthy individuals. The colored representation of samples and probes is ordered by their similarity with a dendogram on top (clustering of samples) and on the right side (clustering of probes) (A). Volcano plot was drawn for comparison of miRs between NSCLC patients and healthy individuals. The two most dysregulated miRs are highlighted in blue on top right (B).</p

Representative immunohistochemical ALCAM stains of primary pancreatic cancer (PAC) lesions.

<p>(A) and (B) strong ALCAM expression, (C) and (D) medium and (E) no expression. (F) Healthy pancreatic tissue. (G) Complete scan of the PAC tissue microarray.</p

Kaplan-Meier overall survival analysis.

<p>(A) Immunohistochemical ALCAM staining of primary pancreatic cancer specimens and (B) low and high s-ALCAM serum levels (patients who died during the first 30 days after surgery were excluded).</p

Patient characteristics.

<p>Patient characteristics.</p

PGK1 and CXCR4 expression, proliferation and inhibition of CXCR4 of neuroblastoma cell lines.

<p>Kelly (<b>A</b>) and SH-EP Tet-21/N (<b>B</b>) neuroblastoma cells were immunostained for PGK1 and CXCR4 expression (<b>Immunohistochemistry</b>). Both cell lines show a positivity for CXCR4 and react to treatment with 20 µg AMD3100 with an inhibition of proliferation (<b>MTT-assay</b>), although only SH-EP Tet-21/N cells reach a significant level of growth reduction. On examination of PGK1 protein expression levels (<b>Western blot</b>) after 48 h of CXCR4 receptor inhibition, treatment with 20 µg AMD3100 leads to a downregulation of PGK1 protein (45 kDa) in SH-EP Tet-21/N but not in Kelly cells. Tubulin (55 kDa) served as control.</p

Overall Survival.

<p>For Kaplan-Meier survival analysis patients were grouped according to positive and negative PGK1 expression. All patients that died during the follow-up period showed positive PGK1 expression, while none of the PGK1 negative patients died. Overall survival of neuroblastoma patients with a PGK1 negative expression was significantly better than that of PGK1 positive patients (<i>p = 0.003</i>).</p