Targeting cell division protein CDK2 could boost immunotherapy response across a wide range of cancers
New research from Dana-Farber Cancer Institute scientists suggests that cyclin-dependent kinase 2 (CDK2) inhibitors, which are currently being tested as treatments that slow the growth of a narrow range of cancers, could potentially be more broadly applicable to a wide range of cancers when combined with immunotherapy.
Scientists from Dana-Farber Cancer Institute have discovered that targeting the cell division protein CDK2 could enhance the effectiveness of immunotherapy across various cancers. CDK2 inhibitors, currently being tested as cancer treatments, could be more broadly applicable when combined with immunotherapy. Studies in animal models showed that a combination of CDK2 inhibitors and immune checkpoint inhibitors led to the eradication of colorectal and breast cancers.
CDK2, activated by cyclin E, is crucial for cell division and can contribute to resistance to immune checkpoint blockade. Inhibition of CDK2 reduces tumor resistance to immunotherapy and enhances dendritic cell activity, promoting the presentation of tumor antigens to T cells. The findings suggest that CDK2 inhibition could be a promising strategy to improve immunotherapy outcomes in a wide range of cancers, including bladder, ovarian, uterine, colorectal, liver, lung, lymphoma, melanoma, and prostate cancers.
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