The galectin family of beta-galactoside binding lectins is involved in normal and pathological processes. Altered expression of galectin-3 has been described in many cancers, and studies of cancer cell lines have implicated this lectin in various aspects of the tumorigenic cascade. The goal of this report was to directly assess the importance of galectin-3 in tumor biology by introducing the galectin-3 null mutation (galectin-3(-/-)) into mouse lines genetically programmed to develop cancers. We used two mouse models of human intestinal cancer, the Apc(Min) and Apc(1638N) lines, to study tumor initiation and tumor progression. We also crossed the galectin-3(-/-) mice with PyMT transgenic animals, a model in which primary mammary gland tumors give rise to lung metastases at high frequency. Unexpectedly, we show that the absence of galectin-3 does not affect the evolution of the disease in any of these three situations.