Julie M. Collins, MD, MPH, discusses the rationale for CDK4/6 inhibitors in endocrine receptor-positive breast cancer.
Julie M. Collins, MD, MPH, an assistant professor at Georgetown University and medical oncologist at MedStar Health, discusses the rationale for CDK4/6 inhibitors in endocrine receptor (ER)–positive breast cancer.
Tumor cell proliferation in many breast cancers is driven by the hyperactivity of the cyclin D–CDK4/6 pathway, says Collins. By blocking this pathway with CDK4/6 inhibitors, the tumor cell proliferation can decrease and prevent these cells from progressing from the G1 phase to S phase of the cell cycle causing cell cycle arrest and a type of cell synesis, according to Collins.
CCND1, which encodes cyclin D, is expressed in high levels in ER-positive breast cancers, adds Collins. CDK4/6 inhibitors have shown strong synergy with antiestrogen therapies, which are used in ER-positive breast cancers. That is the rationale to combine these therapies when treating patients with metastatic ER-positive disease, concludes Collins.