In patient-derived xenografts (PDX) models of advanced prostate tumors, SLC35F2 expression was correlated with intratumoral androgen levels in three models and with expression of constitutively active AR splice variants in a fourth, while androgen-withdrawal via castration of tumor-bearing mice reduced SLC35F2 expression, all consistent with regulation of SLC35F2 by AR axis signaling. This evidence concerns the gene AR and prostate neoplasm.