This study investigates the effects of mistletoe lectin-I (ML-I) on melanoma growth and spread in vivo. The human melanoma cell line MV3 was xenografted into severe combined immunodeficient mice and vehicle solution or purified ML-I was administered at 30, 150 and 500 ng per kg body weight (20 mice per group) daily. After 19 days, mice were killed, primary tumours (PTs) and lungs were dissected out, and tumour weights, number of lung metastases (LMs), number of tumour-infiltrating dendritic cells (DCs), and apoptosis rates in the melanoma cells and in the DCs were assessed. A 35% reduction of PT weight (P ¼ 0.03) and a 55% decrease in number of LMs (P ¼ 0.016) were evident for low-dose ML-I (30 ng kg À1 ) treatment but not for higher doses. Mistletoe lectin-I increased apoptosis rates in the melanoma cells of PTs at all doses, while no induction of apoptosis was noted in the LMs. Low-dose ML-I significantly increased the number of DCs infiltrating the PTs (Po0.0001) and protected DCs against apoptosis, while higher doses induced apoptosis in the DCs (Po0.01). Our results demonstrate that low-dose ML-I reduced melanoma growth and number of metastases in vivo, primarily due to immunomodulatory effects.
Despite the small number of patients and a relatively short follow-up, the present data underline the value of ESD, especially in case of curative resections in the definite and less invasive therapy of EBAC. Attention should be drawn toward subsquamous extension of EBAC requiring a sufficient safety margin as an obligate condition for curative R0 resections. Due to the required learning curve and the management of potential complications, ESD should be restricted to greater endoscopic centers.
Objective: The purpose of this retrospective study was to monitor hypertrophy of future liver remnant following portal vein embolization (PVE) before planned extended right hepatectomy. However, because individual responses to PVE are highly variable, our focus was to identify cofactors of successful hypertrophy. Methods: 28 patients with primary or secondary liver tumours, mean age 64.1 6 12.9 years, underwent PVE. Volumetric analysis of hypertrophy before and after PVE (median 39.0 6 15.7 days) was performed. The embolized liver segments were investigated for occurrence of reperfusion of their portal branches. Blood parameters before PVE were additionally investigated. Results: Patients were divided into responders (21/28) and non-responders (7/28) by post-PVE standardized future liver remnant being above or below 25%, respectively. No significant differences between the groups were found regarding biometric and volumetric parameters before PVE. In the entire group after PVE, the mean absolute increase of Segments 2 and 3 was 196.0 6 84.7 cm 3 and the median relative increase was 46.6 6 98.8%. The formation of left to right hepatic portoportal collaterals exhibited a negative correlation to successful hypertrophy (p 5 0.004) as well as low plasma total protein (p 5 0.019). Successful embolization of Segment IV showed only a trend to significance (p 5 0.098). Conclusion: Cofactors associated with a favourable outcome regarding hypertrophy were the absence of collaterals in the control CT scans and high plasma total protein.
Advances in knowledge:Portoportal collaterals negatively influence hypertrophy after PVE. On the other hand, plasma total protein is a positive prognostic indicator on hypertrophy of the liver in our cohort.
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