Contain phytochemicals and other pharmacologically active ingredients linked to chronic diseases. Moreover the functional polymorphism K172N appears to be a risk factor for alcohol intake and dependence. This variant is very rare in Caucasian populations and therefore its genotyping was not attempted in this sample set. TAS2R16 genetic variants have also been associated with the development of nicotine dependence in African Americans. These observations point to a role of variation in the TAS2R16 receptor in recognizing and therefore modulating the effect of both beneficial and harmful molecules with which the organism interacts during life. It is possible that the fine tuning of the receptor function due to the genetic polymorphisms along with the environment may modulate how many beneficial and how many harmful compounds are recognized by the receptor throughout the life span and that this could, in the long term, modify the chances to reach very old ages. However there is also another possible, even though highly speculative, explanation of the involvement of TAS2R16 genetic variability in healthy aging. Numerous recent reports investigated non-gustatory actions of taste receptors. They have been shown to be expressed in a plethora of tissues such as the respiratory system where they affect respiratory functions in response to noxious stimuli. Recently it has been shown that taste receptors are expressed also in the testis in mouse, where they can be involved in spermatogenesis. The emerging picture is therefore that taste receptors could behave as pleiotropic genes, whose products are used by various cells, or have signaling function on various targets not linked one to the other. Probably the bitter sensing is just one of the functions performed by this cluster of genes, which could have a central role in the homeostasis of the organisms. Therefore their genetic variations can affect profoundly various traits, including longevity, in a way that we are just beginning to understand. Major advances have been made in the treatment of breast cancer; however, it still remains the leading cause of Pazopanib cancer death among women worldwide. In the United States breast cancer is the second leading cause of cancer death among women after lung cancer. The chemotherapeutic drug etoposide is used as a salvage treatment for advanced stage breast cancer and causes DNA damage by stabilization of DNA topoisomerase II. Etoposide stabilizes the topoisomerase II DNA covalent complex impairing the strand-rejoining activity of the enzyme causing double stranded DNA breaks to persist instead of being repaired. Etoposide can delay progression of the cell cycle through the late S or early G2 phase but has no effect on tubulin assembly. As a single agent, oral etoposide response rate for breast cancer was found to be around 35% and the mean bioavailability of orally administered etoposide is approximately 50%. In a more recent study, it was found that oral etoposide in combination with cisplatin was much more effective in patients with advanced breast cancer than paclitaxel. Etoposide is also widely used for the treatment of small cell lung cancer, lymphoma, leukemia and testicular cancer among others. Though etoposide is widely used as therapy for cancer patients, the fact remains that tumors often acquire resistance to the drug. The nature of drug resistance is inherently multi-factorial involving mechanisms which include alteration in drug targets, inactivation/detoxification of the drug, decreased drug up take, increased drug efflux and the disregulation of the apoptotic pathway.