抄録
Metastasis is a life-threatening disease that accounts for as much as 90% of cancer-related mortality. Carcinoma cells have often spread to distant organs at the time patients present with cancer. Routine clinical examinations have produced significant progress in detecting metastasis but existing methods for screening cancer patients are incapable of detecting micrometastasis and disseminated tumour cells (DTCs) in distant organs. Adjuvant chemotherapy and adjuvant radiotherapy are anticipated to prevent relapse and death. However, over periods of time ranging from years to decades, these metastatic cells residing in distant organs often relapse, corrupt the local microenvironment and acquire the ability to develop into macrometastases. Metastatic nodules are known to be formed by carcinoma cells harboring increased numbers of epi/genetic alterations conferring aggressive and drug-resistant propensities. In addition, more recently emerging evidence supports the notion that the tumour-associated stroma, consisting of endothelial cells, leukocytes, macrophages, myofibroblasts, bone marrow-derived progenitors and abundant extracellular matrix (ECM), significantly facilitates tumour metastasis. The molecular signalling underlying the complexity of heterogeneous stromal-tumour interactions that is relevant to tumour metastasis is the subject of intensive research. The tumour-associated stroma, in addition to tumour cell-autonomous alterations plays significant roles to instigate and support progression of the multi-step processes of tumour metastasis.
