However, the feasibility to target actin is shown here in an in vivo mouse model of tumor metastasis. Herein, treatment with Chondramide diminishes the metastasis of mammary cancer cells to the lung significantly. As migration is reduced at lower concentrations and shorter time points than nuclear fragmentation occurs, we propose that the inhibitory effect on metastasis is not due to an apoptotic effect but the abrogation of migration and Chloroquine Phosphate invasion. The dose of 0.5 mg/kg was well tolerated as the body weight of treated mice stayed constant throughout the observation period. Although there is still room for further development, e.g. specific targeting, we could show a pharmacological effect for Chondramide on metastasis in vivo without acute toxicity. In our in vivo treatment regime we tried to keep close to a potential clinical setting, and, thus, chose systemic administration of Chondramide. This, of course, means that cells other than tumor cells might have been affected by the compound, and that we cannot dissect, which step of metastasis might have been primarily affected. Due to the short presence of compound, it is unlikely that later steps of 
metastasis formation might have been influenced by Chondramide. As therapies against cancer metastasis are still missing, more efforts need to be made in research addressing metastatic cancer cells. This work provides evidence that actin is a suitable target to inhibit cancer cell migration, and gives first insights into underlying mechanisms. Combining actin binding natural compounds with specific targeting strategies could lead to a powerful weapon to treat tumor metastasis. Personalizing or tailoring health care to the individual patient’s need and genetic makeup gains more and more importance in daily practice. It is especially rewarding in the setting of therapies associated with severe side effects but also with high costs. Reliable biomarkers, that either predict response to therapy or risk of side effects, are a prerequisite for this approach. In case of unfavorable predictors addition or the sole use of adiuvants with no or only marginal side effects but also cost may be a valuable approach. Adjuvant interferon alpha treatment in melanoma fulfills the criteria for a therapeutic approach for which such a biomarker would be highly desirable: Several studies support the therapeutic efficacy in terms of disease-free survival and to a lower extent overall survival. This potential benefit is counteracted by the fact that interferon alpha has to be taken for many months and is often associated with side effects that affect patients’ quality of life. Interferon alpha is used in several clinical settings. One main indication is the treatment of acute and chronic hepatitis C infection. Also in this application response to interferon is far below 100% and side effects are very common. However in this setting a biomarker �C IL28 C/T dimorphism rs12979860 – predicting the probability to reach sustained virologic response has recently been identified by genome-wide association studies. Analysis of this SNP has become Ginsenoside-Ro common practice and helps clinicians to either encourage their patients to undergo therapy or to defer treatment. Patients showing the favorable CC genotype have up to a twofold higher rate of SVR and higher rates of early virologic response than non-CC patients. Another type III interferon, interferon l4, was described recently as inducer of ISGs and has a similar prognostic value regarding treatment response. The mechanism underlying the influence of IL28B polymorphism on the response to interferon alpha treatment is not known. IL28B is a type III interferon. Type I and type III interferon act via different receptors, but activate the same signal cascades and have similar effects.