AuthOr’s VIew AuthOr’s VIew

Breast carcinoma is the primary cause of cancer-related death in women. Mortality mainly ensues the metastatic spread of tumor cells to other organs, which involves the acquisition of invasive features by malignant cells as well as their ability to elude antitumor immune responses.1 Breast tumors employ diverse strategies to thwart the attacks of the immune system and create a tolerogenic microenvironment, including the production of immunosup-pressive cytokines such as transforming growth factor β (TGFβ) and interleukin (IL)-102 as well as the expression of pro-apoptotic molecules including FAS ligand3 and TRAIL,4 which may act in concert to dampen the activity of effector T cells. In addition, accumulating evidence high-lights the importance of regulatory cell populations,5 including myeloid-derived suppressor cells (MDSCs), regulatory T cells (Tregs), tolerogenic (plasmacytoid or myeloid) dendritic cells (DCs) and the recently-discovered adipose-derived stem cells (ASCs).6 These immunosuppressive mechanisms can either be pre-existing, arise through the outgrowth of escape tumor variants, or be established in the course of immunoediting, namely, the pro-cess whereby the immune system “sculpts” the tumor by eliminating some, but not all, malignant cells.1 It has been proposed that the blockade of these immunosup-pressive mechanisms might be effective in Thwarting galectin-induced immunosuppression in breast cancer Mariana salatino, * tomas Dalotto-Moreno and Gabriel A. rabinovic