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Instead of repressing tumor-suppressor genes, this form of EZH2 drives rapid protein production and activates growth factors like TGF-β, fostering an environment around the tumor that promotes cancer progression despite androgen receptor inhibition.

For example, females with a DSD known as androgen insensitivity syndrome have XY chromosomes; they produce testosterone; but their bodies aren’t equipped to process it.

In other words, inhibiting the function of the androgen receptor alters the regulation of genes within cells, allowing for the expression of genes that are normally silenced and the alteration of the cell state.

The first, published in Nucleic Acids Research, explored how the glucocorticoid receptor replaces the androgen receptor on the molecular level.

Current treatment methods for prostate cancer include androgen ablation, chemotherapy, radiotherapy and radical prostatectomy, but are ineffective against advanced prostate cancers.