The fact that metastasis is site specific is known for almost 150 years but ignored by many cancer researchers and clinicians. The interactions between cancer cells and the microenvironment of future metastatic sites are significant players in the metastatic cascade but many cellular and molecular determinants leading to site-specific metastasis await discovery. Elucidating the mechanisms underlying organ specificity of metastasis is of prime importance not only in basic cancer research but mainly in precision (personalized) medicine. Circulating tumor cells disseminate to future metastatic sites. Interactions with the microenvironment of these sites may lead to the formation of dormant micrometastasis. The micrometastases remain in a state of dormancy until “awakened” to progress towards overt metastases. The mechanisms that maintain dormancy of disseminated tumor cells in a certain metastatic microenvironment and those that awaken the dormant micrometastases, driving their progression towards frank metastasis, are still obscure. It is clear, however, that the metastatic microenvironment plays a major role in these events. Three topics will be discussed in this presentation: (1) Indications that the same type of microenvironmental cells in different organs may display a different molecular profile and that metastases originating from a single tumor that develop in different organ microenvironments may express different characteristics. (2) Cancer cells hijack physiological mechanisms operating in a particular organ to form and sustain metastasis in that organ. (3) Interactions between metastatic cells with the metastatic microenvironment may be bidirectional ie, promote or antagonize metastasis formation. Here we will report on a novel microenvironment-derived anti metastasis factor.
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