No animals were specifically generated for this study. Samples were obtained from fetuses generated by artificial insemination after estrus cycle synchronization and by in vitro fertilization procedures and embryo transfer as described previously. Fetuses generated by in-vitro fertilization with embryo culture were classified as overgrown when their weight exceeded the mean of control fetuses conceived in-vivo by more than four standard deviations. Brain samples were from the upper-left hemisphere of the telencephalon, liver samples from the Lobus hepatis sinister, and skeletal muscle samples from the Musculus gluteus maximus. Lung samples were obtained from the tip of the lungs and heart muscle was collected from the apex of the heart. The kidney sample consisted of one half of a bisected kidney. Multiple myeloma is a lymphoid neoplasm characterized by infiltration in the bone marrow of malignant plasma cells. The presence of monoclonal immunoglobulins and defective innate or adaptive immune responses render MM patients vulnerable to infectious or inflammatory conditions, and in most cases these complications hamper the therapeutic approaches. Furthermore, a history of infectious and chronic inflammatory diseases has been reported in variability mdd crhr1 gene antidepressant response mdd certain MM patients. Thus, contribution of inflammatory or infectious conditions to MM pathogenesis or progression seems plausible; however, the underlying molecular mechanisms have not been clearly deciphered. Indeed the link between inflammation and malignant conditions has long been pursued by many researchers. In recent years, Toll-like receptors, which are instrumental in integrating the innate and adaptive immune responses, have been addressed as the potential linking elements. These receptors have been detected in many cancer cells with various functional responses following their triggering. In MM, TLRs have been reported to be expressed heterogeneously on freshly isolated myeloma cells and MM cell lines, and their expression is significantly higher than on normal plasma cells. However, most of the analyses have been limited to mRNA level showing inconsistencies in TLR patterns expressed by MM cells and the cellular responses following their triggering. Consequently, information on the functional protein expression patterns of these molecules is limited. Here, we present a comprehensive study on the expression profile of TLRs on established and commonly used human myeloma cell lines and MM primary cells. We show strong expression of TLRs in primary MM cells as well as in all MM cell lines, which indicates a propensity for responding to tumor-induced inflammatory signals, which seem inevitable in the MM bone marrow environment. Quantitative PCR was performed for the expression of TLR3 mRNA in Fravel, L363 and NCI- H929. 500 ng total RNA from indicated cell lines was transcribed using a first strand synthesis kit. Two microliters from each sample was applied to SYBR green real time PCR using primers which were as described previously. The beta actin primer was described above. Standard curves for targets and beta actin genes were created with two-fold dilutions of a measured concentration of pooled cDNA. The amount of amplicon for each gene in samples was then determined using log of concentration and slope of the curve and normalized to that of actin. The expression of TLRs on cells of B-lymphoid malignancies, MM and CLL, has been documented in different recent studies. These studies, however, show inconsistencies in TLR patterns expressed by MM cells and the cellular responses following their triggering. This is the first study in which TLR expression in different HMCLs and primary MM cells has been evaluated at mRNA and protein level.