Rb's unexpected activation of estrogen-responsive genes could explain breast cancer treatment resistance
Researchers at Peter Mac have discovered why breast cancer treatment stops working for some patients, uncovering the unexpected role of one of the body's most important cancer-fighting proteins. The study, published in Nature, revealed that the retinoblastoma (Rb) protein—long considered one of the body's natural brakes on cancer growth—has a more complex function than previously understood.
Researchers at Peter Mac have discovered an unexpected role for the retinoblastoma (Rb) protein in breast cancer treatment resistance. While Rb is typically viewed as a tumor suppressor that prevents uncontrolled cell division, a study published in Nature reveals it can also activate estrogen-responsive genes. In hormone receptor-positive (HR+) breast cancer, CDK4/6 inhibitors restore Rb's growth-arrest capabilities by switching it back on.
However, when tumors become resistant to endocrine therapy, the estrogen-related gene program continues despite treatment, diminishing the effectiveness of CDK4/6 inhibitors. This dual function of Rb - suppressing cell division while activating estrogen-responsive genes - provides new insights into drug resistance and the broader role of tumor suppressors in breast cancer.
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