Background Myxoid liposarcoma accounts for 40% of all liposarco mas and occurs most commonly in the extremities. In about 95% Colorectal cancer of cases, myxoid liposarcoma is cytogen etically characterized Inhibitors,Modulators,Libraries by t, creating a chimerical FUS DDIT3 gene which has been thought to play a pivotal role in its tumourigenesis. The cor nerstone of curative treatment for myxoid liposarcoma is surgery with an overall 10 years survival of 80%. Prog nosis is mainly determined by the percentage of round cell component of the tumor. Myxoid liposarcoma with more than 5% round cell component are defined as high grade and prone to metastasis. Treatment options for patients with inoperable or metastatic dis ease are relatively poor, though trials with new drugs reveal good perspectives for the future.

Therefore, clinical trials to test and validate new treatment options for liposarcoma Inhibitors,Modulators,Libraries subtypes are necessary. Nowadays, adjuvant chemother apy of liposarcoma patients is limited with only ifosfamide and anthracyclins showing 20 40% response rates in untreated patients. Trabectedin is a novel chemotherapeutic agent derived from the marine tunicate Ecteinascidia turbinate. By binding to the DNA minor groove, ET 743 forms covalent adducts with the N2 position of guanine through its car binolamine moiety. As a result, the minor groove bends toward the major groove. The cytotoxic activity of ET 743 is largely Inhibitors,Modulators,Libraries based on its interaction with nucleoside excision repair machinery, as well as through the induc tion of double strand breaks.

Phase I and II stu dies showed promising results in myxoid liposarcoma Inhibitors,Modulators,Libraries patients with advanced Inhibitors,Modulators,Libraries disease though recent studies reported an increasing number of side effects. During the last years, tumor specific targeted therapy has shown to be effective in many cancers, including sarcomas. Especially kinase inhibitors are an emerging class of small molecule inhibitors that target unique kinase conformational forms and binding sites. Notable advantages are higher specificity and generally more manageable and reversible side effects. This necessitates the study of separate soft tissue tumour entities. In the present study, we explored the acti vated pathways in myxoid liposarcoma cells using kinome profiling to find new treatment possibilities. Kinases phosphorylate tyrosine, threonine or serine resi dues on proteins, thereby serving as a switch to activate pathways involved in cell cycle, cell survival and differentiation. Moreover, kinases are selleck U0126 promising targets for anti cancer therapy as they do not require new pro tein synthesis, therefore act rapidly and are also promis ing in slow cycling tumors. Data on activated pathways in myxoid liposarcoma are sparse.