Breast cancer-cell models that were rendered resistant to methotrexate by prolonged exposure to the drug also displayed enhanced expression of several UGT1As—particularly UGT1A6—as well as enhanced glucuronidation activity.47 This effect was not observed in colorectal, pancreatic, leukaemia and osteosarcoma models made resistant to methotrexate in a similar manner,47 suggesting that UGT-dependent mechanisms of resistance might be specific to some cancer-cell-drug contexts and might be related to the specific UGTs that are expressed in the target organ. This evidence concerns the gene SLC35A2 and cancer.