An extensive body of information supports the concept that, in analogy to tumor growth at the primary site, the transition of tumor micrometastasis to exponential growth AZD5363 in distant organs is also angiogenesis dependent and can thus be efficiently inhibited by anti angiogenic agents. Thus, it’s plausible that even when anti angiogenic treatment fails to prevent the dissemination of invasive tumor cells or to provide a particular advantage for tumor cells having an increased ability to invade into surrounding tissue and distant organs, anti angiogenesis will still provide a robust technique to prevent the transition of dormant micro metastasis to rapidly growing angiogenic macrometastasis. This is especially essential since emerging data suggest that distribution of tumor cells in distant organs and adjacent buildings might constitute a really early event in the tumorigenesis process of some cancers, such as for example breast cancer. Therefore, along with local beneficial tumefaction results, the prevention of the angiogenic switch in dormant micrometastasis provides still another rationale for adjuvant anti angiogenic therapy in local or locally advanced cancer. Nevertheless, the early distribution of tumor cells into different microenvironments in remote areas also suggests the possibility of parallel development of the primary and metastatic tumors. This will have important implications Gene expression for anti angiogenic therapy. For example, it remains to be elucidated if the variety of selection constraints in different metastatic niches can lead to variations in the angiogenic profiles of, for example, primary vs. metastatic tumors or between tumors from different metastatic sites. Consequently, might such variety lead to evasion of metastatic tumors from anti angiogenic therapy that targets the angiogenic profile of the primary tumor Maybe there is a possibility to synchronize the tumors at different web sites to become influenced by a particular angiogenic profile The study of tumor micro metastases and the temporal structure of the angiogenic switch of dormant tumors are often restricted due to the failure of local tumor get a handle on and therefore small success or observation periods. But, with the advent of improved local therapy sessions and molecular biology, the area of disseminated tumor cells and tumor micro metastasis is growing very rapidly. The molecular mechanisms underlying the period and the change of these tumor cells into an angiogenic fastgrowing state are becoming the focus of cancer CX-4945 structure research. For example,howdoes an effective local treatment change the blood flow levels of endogenous antiangiogenic proteins produced by primary tumor Could a decrease in the era of anti angiogenic proteins by the primary tumor help the development of distant metastases Despite recent advances, the field of tumor metastasis remains in an early stage of development and needs considerable attention.