A recent publication in Cell reveals that oral administration of agonists to LXR, a nuclear hormone receptor, caused transcriptional induction of tumoral and stromal ApoE and subsequent reduction in tumor size of up to 80% in metastatic melanoma. More importantly, activation of LXR demonstrated the tumor-suppression cooperatively with anti-CTLA-4 antibody and other frontline regimens, establishing LXR as a therapeutic target for melanoma.

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