Brain cancers have high mortality compared to other cancer types. One of the most frequent brain cancer types are the high grade glioma. More than 50 % of all glioma diagnoses are glioblastoma multi-forme (GBM), which is highly infiltrative and exceedingly vascular. The prognosis for GBM is poor de-spite optimal treatment, with a mean survival of 12-15 months. The traditional treatment regimen for GBM has focused on surgical removal of tumour mass fol-lowed by adjuvant radio- and chemotherapy. Recently, progress in the understanding of tumourigene-sis has promoted development of molecular targeted drugs, such as receptor tyrosine kinases inhibi-tors and antiangiogenic agents. However, implementing these novel drugs in GBM treatment have only resulted in modest improvements of prognosis for the patients. A strategy to further optimise GBM treatment is to apply drug carriers for the transport of chemo-therapeutic agents, enhancing accumulation of drug in the tumour and diminishing unspecific side effects. Liposomal drug carriers have some advantages compared to other drug carrier systems, and are therefore a good choice for the delivery of chemotherapeutics. Caelyx, doxorubicin-loaded lipo-somes, has so far been approved for the treatment of AIDS-related Kaposi’s sarcoma, metastatic breast cancer, advanced ovarian cancer and multiple myeloma. Currently, Caelyx is in phase II clinical trials investigating its application in GBM therapy. Preclinically, the effect of modifying doxorubicin liposomes with antibodies or ligands targeting specific molecules on either the tumour cells or the tumour vasculature has been investigated exten-sively. In GBM animal models, targeted doxorubicin liposomes have demonstrated improved antican-cer effects compared to untargeted liposomes and free drug. Due to previous success in targeting of tumour cells and tumour vasculature separately, we hypothesise that combining these two approaches will result in synergistic effects. This could lead to improved anticancer effects and reduced toxicity in GBM treatment. In this study transferrin receptor and vascular cell adhesion molecule-1 (VCAM-1) antibodies are investigated for their potential to serve as specific ligands for liposome targeting to GBM and endothe-lial cells, in vitro. The expression of transferrin receptor by the human GBM cell line, U87-MG, as well as the expression of VCAM-1 by the murine endothelioma cell line, bEnd.3 were tested by western blotting and immunocytochemistry. Liposomes conjugated with transferrin receptor antibody, VCAM-1 antibodies and serum proteins were prepared together with unconjugated liposomes. The internali-sation of liposomes in both U87-MG and bEnd.3 cells was visualised using fluorescence microscopy, and the intracellular liposome quantity was investigated through Fluorescent-Activated Cell Sorting (FACS) analysis. Expression of target proteins by U87-MG and bEnd.3 was neither confirmed by western blot nor immunocytochemistry. Fluorescence microscopy showed that liposomes were internalised in both cell types. FACS analysis showed a slightly higher uptake of monoclonal antibody (mAb) transferrin receptor-conjugated liposomes compared to serum protein-conjugated liposome, whereas a higher uptake of mAb VCAM-1-conjugated liposomes was not found. In conclusion, further research is needed to reveal the potential of transferrin receptor and VCAM-1 as targets in the liposomal treatment of GBM.