How do tumor stem cells actively escape from host immunosurveillance?

Tumor stem cells (TSCs) are considered as the "seeds" in tumor development, metastasis and recurrence. Despite the various immunosurveillance mechanisms in the host, TSCs may possess the phenotypic and functional properties to evade host immunosurveillance and immune-mediated rejection in immunologically intact individuals. The mechanisms of TSC recognition and their consequent destruction are actively disturbed by various processes, including altered immunogenicity of TSCs, production of TSC-derived regulatory molecules, and interaction of TSCs with tumor-infiltrating immune cells. In addition to these TSC-mediated mechanisms, the diverse mesenchymal cells and cytokines in the tumor microenvironment are contribute to TSC immune escape. Recent mechanistic studies provide a more comprehensive understanding of TSCs in the biology, prevention, and therapy of solid tumors. This review will focus on the latest findings for mechanisms underlying TSCs' escape from the attack of immune system.

[Assessment of hemodynamics in patients with Budd-Chiari syndrome after interventional treatment].

OBJECTIVE: To study the changes in morphology of liver and spleen and hemodynamics of the patients with Budd-Chiari syndrome (BCS) after interventional treatment. METHODS: The dimensions of liver and spleen were detected by routine ultrasonography in 30 normal control subjects and 256 BCS patients before and after inventional therapy. Color duplex sonography was employed to measure the hemodynamic changes. RESULTS: Compared with the control group, BCS patients before interventional therapy showed obvious liver and spleen enlargements (P<0.005), specially the caudate lobe of the liver (P<0.001), which were significantly reduced 7 days after interventional treatment (P<0.005), but the spleen was still larger than that of the control group (P<0.005) even till 6 months after the therapy. Color Doppler flow imaging (CDFI) revealed local high-speed blood flow in patients with stenosis of the inferior vena cave (IVC), but color flow was not detected in patients with IVC obstruction, who had hepatic vein dilation (P<0.005) with slowed blood flow and collateral formation of in the liver, as well as decreased velocity of blood flow in the portal vein. After interventional treatment, the diameter of the involved IVC increased with blood flow restoration and the size and shape of the stent were detected clearly. The velocity of blood flow was increased in both the hepatic and portal veins (P<0.005). CONCLUSION: Interventional therapy can relieve obstruction of blood flow in the liver and improve the hemodynamics of patients with BCS.

Clinical significance and prognostic value of Vav1 expression in Non-small cell lung cancer.

Vav1 has been reported to be involved in human cancers, however, the expression and clinical significance of Vav1 in NSCLC are not fully understood. In the present study, we examined the expression of Vav1 in 170 NSCLC patients who underwent radical resection by the immunohistochemical analyses. The association between the Vav1 expression and clinicopathological variables was analyzed. The multivariate Cox proportional hazards model was conducted to determine the prognostic value of Vav1 on the long-term survival. The results showed that the elevated Vav1 expression was correlated positively with lymph node metastasis (P<0.001), T stage (P<0.001) and poor histological differentiation (P<0.001). Patients with negative or low Vav1 expression had better prognoses than those with high Vav1 expression (P<0.001). Multivariate analysis indicated that Vav1 was independent prognostic factor for overall survival (OS) (HR 2.079, 95% CI 1.564 to 2.762, P<0.001) and disease-free survival (DFS) (HR 1.810, 95% CI 1.391 to 2.356, P<0.001). Our findings showed that overexpressed Vav1 was correlated with aggressive tumor behavior. Val1 was an independent factor for NSCLC prognosis, which may serve as a novel prognostic factor and potential target to improve the long-term outcome of NSCLC.