The present findings suggest that RAGE-aptamer could attenuate melanoma growth and liver metastasis in nude mice by suppressing the tumor angiogenesis and macrophage infiltration via inhibition of the AGE-RAGE system.
As miR-21 and miR-200c were abundantly expressed in both metastatic liver sites and primary lesions, we evaluated Ago2-miR-21 as a candidate biomarker of both active export and cytolysis while Ago2-miR-200c as a biomarker of cytolysis in plasma obtained from colorectal cancer (CRC) patients before treatment and in a series of plasma obtained from CRC patients with liver metastasis who received systemic chemotherapy.
High mRNA levels of Arp2, that in situ hybridization revealed to be expressed by the cancer cells, were significantly associated with liver metastasis.
In preclinical mechanistic studies, we found that cancer cell motility mediated by the actin-related protein 2/3 complex (Arp2/3) is required for vessel co-option in liver metastases in vivo and that, in this setting, combined inhibition of angiogenesis and vessel co-option is more effective than the inhibition of angiogenesis alone.
After HA receptor (CD44)-mediated cellular uptake of the HTsRP-NC by the liver cancer cells, functional expression of AKT siRNA leads to the suppression of metastatic liver cancer growth in a colorectal liver metastasis (CLM) murine model.
Similar results were also seen between liver metastases and primary breast tumors [AKT (S473) <i>P</i> < 0.01, mTOR (S2448) <i>P</i> < 0.01, 4EBP1 (S65) <i>P</i> = 0.01].
Induction of the IL-33/ILC2/IL-13 circuit in a murine biliary injury model promoted epithelial repair; however, induction of this circuit in mice with constitutive activation of AKT and YAP in bile ducts induced cholangiocarcinoma with liver metastases.
Suppression of Akt2 expression in highly metastatic colorectal carcinoma cells inhibits their ability to metastasize in an experimental liver metastasis model.
Xenografts established by injecting AKT2 silenced human neuroblastoma cells into murine spleen expressed decreased levels of AKT2 and resulted in fewer liver metastases compared to controls in vivo.
To evaluate late toxicity, the radiation-induced hepatic toxicity (RIHT) was determined by the common terminology criteria for adverse events toxicity grade of bilirubin, aspartate transaminase, alanine transaminase, alkaline phosphatase, and albumin, and was defined from 3 months after RT until liver metastasis was revealed.
The superior predictive value of <sup>166</sup>Ho-scout compared with <sup>99m</sup>Tc-macroaggregated albumin prior to <sup>166</sup>Ho-microspheres radioembolization in patients with liver metastases.
Number of active tumors, performance status, albumin, primary tumor site, prior hospitalizationwithin the last 3 months, and liver metastases predicted overall survival on uinvariate and multivariable analysis (p < 0.05 for all).
In the training cohort (n = 445), performance status, liver metastasis, Carbohydrate antigen 19-9 (CA19-9) log-value, absolute neutrophil count (ANC), and albumin were independent prognostic factors for overall survival (OS).
Lung shunt fraction (LSF) was calculated from macroaggregated albumin scan after transcatheter injection of radioactive particles in 62 patients with colorectal cancer and liver metastases evaluated for selective internal radiation therapy (SIRT) from May 2007 to August 2012.
Significant differences in OS were observed between patients with and without 5 of 7 criteria on univariate analysis: low albumin (P<0.0001), high lactate dehydrogenase (P = 0.002), liver metastasis (P = 0.004), retroperitoneal lymphadenopathy (P = 0.002), and supradiaphragmatic lymphadenopathy (P = 0.019).
Among patients with liver metastasis, inferior OS was associated with low albumin, poor Eastern Cooperative Oncology Group performance status, driver mutation, and number of liver metastasis (≥ 5).