How Prostate Cancers Become Resistant to Androgen Deprivation Therapies Seen in Study

How Prostate Cancers Become Resistant to Androgen Deprivation Therapies Seen in Study
Understanding how prostate cancer cells develop resistance to androgen deprivation therapies is critical to developing therapies that restore sensitivity to such agents, improving the treatment — and the chances — of people with castration-resistant prostate cancer. Researchers recently identified two tumor-suppressor proteins, TP53 and RB1, that are lost in the transition from androgen-dependent to androgen-independent cells. They also found that targeting a protein, which is more abundant after this transition, appeared to help restore cell sensitivity to androgen deprivation therapy (ADT). The study, "Rb1 and Trp53 cooperate to suppress prostate cancer lineage plasticity, metastasis, and antiandrogen resistance," was published in Science. "Androgen-deprivation therapy is commonly used to treat patients whose prostate cancer has spread beyond the prostate. While most men initially respond to this therapy, the cancer nearly always returns and is often aggressive and lethal," David Goodrich, PhD, the study's co-senior author and a professor of Oncology in the Department of Pharmacology and Therapeutics at Roswell Park, said in a press release. "We have discovered a mechanism that causes progression to this aggressive form of prostate cancer, providing a new opportunity to prevent or treat lethal forms of prostate cancer." Prior studies have suggested that lineage plasticity — how a cell adapts to environmental changes — promotes therapeutic resistance, but the mechanisms underlying lineage plas
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Inês Martins holds a BSc in Cell and Molecular Biology from Universidade Nova de Lisboa and is currently finishing her PhD in Biomedical Sciences at Universidade de Lisboa. Her work has been focused on blood vessels and their role in both hematopoiesis and cancer development.

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