Androgen-Targeted Therapy-Induced Epithelial Mesenchymal Plasticity and Neuroendocrine Transdifferentiation in Prostate Cancer: An Opportunity for Intervention

What is it about?

Although targeting the androgen axis has clear therapeutic benefit, its effectiveness is temporary, as prostate tumor cells adapt to survive and grow. The removal of androgens has been shown to activate epithelial–mesenchymal transition (EMT), neuroendocrine transdifferentiation (NEtD) and cancer stem cell-like gene programs. - EMT has established roles in promoting biological phenotypes associated with tumor progression (migration/invasion, tumor cell survival, cancer stem cell-like properties, resistance to radiation and chemotherapy) in multiple human cancer types. - NEtD in prostate cancer is associated with resistance to therapy, visceral metastasis, and aggressive disease. - Cancer Stem Cell phenotypes are associated with disease recurrence, metastasis, and cell survival in circulation as Circulating tumor cells. Thus, activation of these gene programs via inhibition of the androgen axis provides a mechanism by which tumor cells can adapt to promote disease recurrence and progression

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