BACKGROUND: Many primary tumors may cause liver metastases, which are generally treated with surgical resection and/or chemotherapy. After resection of liver metastases in patients with colorectal carcinoma, 5-year survival rates are achieved in 25-38%, and two-thirds of patients will experience recurrent metastases. We examined percutaneous, minimally invasive, laser-induced thermotherapy (LITT) as an alternative outpatient procedure. Local tumor control rate and survival data were analyzed prospectively. METHODS: Between June 1993 and August 2000, 7148 laser applications were performed in 1981 lesions in 705 consecutive patients and 1653 treatment sessions. The complications of the procedure were evaluated by clinical examination and magnetic resonance imaging (MRI) and computed tomography. Local tumor control was evaluated by plain and contrast-enhanced follow-up MRI using T1- and T2-weighted spin-echo and gradient-echo sequences every 3 months after treatment. Cumulative survival times were calculated using the Kaplan-Meier method. RESULTS: The overall rate of complications and side effects was 7.5%. The rate of clinically relevant complications was 1.3%. Local tumor control rate after 3 months was 99.3%; 6 months after laser treatment, plain and contrast-enhanced MRI documented a local tumor control rate of 97.9%. In patients treated with MR-guided LITT for unresectable colorectal liver metastases, the mean survival was 41.8 months (95% confidence interval = 37.3-46.4 months). The 1-year survival rate was 93%, the 2-year survival rate was 74%, the 3-year survival rate was 50%, and the 5-year survival was 30%. In patients treated with LITT for liver metastases from breast cancer, the mean survival was 4.3 years (95% confidence interval = 3.6-5.0 years). CONCLUSION: In patients with liver metastases, local tumor destruction using minimally invasive, percutaneous LITT under local anesthesia results in improved clinical outcomes and survival rates and can be a potential alternative to surgical resection.

Adult↗

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Decreased T cell stimulatory capacity of monocyte-derived human macrophages following herpes simplex virus type 1 infection.

Macrophages play a central role in establishing a specific immune response by acting as professional antigen presenting cells (APC) for T cells leading to a vigorous immune response. In order to analyze if Herpes simplex Virus (HSV) type 1 infection might affect the macrophage APC-function, monocyte-derived human macrophages were infected with HSV-1 strain F in vitro. Cocultures with allogeneic T cells revealed a strongly impaired stimulatory capacity of HSV-infected macrophages compared to uninfected controls which was not owing to a productive viral infection in macrophages. An increased expression of Fas ligand (FasL/CD95L) was detected in HSV-infected macrophages by FACS analysis. Although the majority of the macrophages expressed high levels of Fas (CD95/Apo-1), the HSV-induced upregulation of FasL did not result in an increased autocrine apoptosis of macrophages which might be related to endogenous expression of the apoptosis inhibitor FLICE inhibitory protein (FLIP). However, substantial apoptosis occurred in peripheral T cells as well as Fas-sensitive Jurkat T cells when cocultured with HSV-infected macrophages. These findings suggest that the paracrine killing of activated T cells by FasL expressing APC might be a novel strategy of immune evasion by HSV.

Apoptosis↗