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Metastatic spread is the main cause of cancer-related mortality, the lung is the main part of metastatic seeds. The treatment available for patients with metastatic disease is very limited. Therefore, there is an urgent need to prevent or limit new strategies for metastatic transmission and treatment of existing transfers. Metastatic cascades are very complex and are affected by multiple factors associated with the tumor cell itself and the microenvironment of the future metastatic site. We hypothesize that changing the lung microenvironment by preventing the central ubiquitous signal may affect metastatic seeds in the lungs. In view of the basal level of advanced glycation end products (RAGE) receptors in lung tissue and their proinflammatory properties, we investigated the effects of interfering with their ligands; high mobility group Box 1 (HMGB1). To this end, we tested the effect of a HMGB1 antagonist carboplatin on the growth and metastasis of primary tumors in several mouse tumor models. We show that antagonism of HMGB1 prevents adhesion and colonization of cancer cells in the lungs by in vitro and in vivo adhesion and cell-cell interactions. We demonstrate that these activities are mediated by downregulation of the adhesion molecule adhesion molecule 1 (ICAM1), resulting in a reduction in metastatic burden. Carbohydrates can significantly reduce the formation of lung metastases, can be used as a preventive treatment of metastatic.