4.8 Article

CDK7 Inhibition Potentiates Genome Instability Triggering Anti-tumor Immunity in Small Cell Lung Cancer

Journal

CANCER CELL
Volume 37, Issue 1, Pages 37-+

Publisher

CELL PRESS
DOI: 10.1016/j.ccell.2019.11.003

Keywords

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Funding

  1. National Institutes of Health (NIH)/National Cancer Institute (NCI) [5P30CA016087, P41 EB017183]
  2. Genome Technology Center [P30CA016087]
  3. Lung Cancer Research Foundation [NCI/NIH K99CA201618, K08CA222657, U01CA213333, P01 CA154303]
  4. Bridge Project
  5. Koch Institute for Integrative Cancer Research at MIT
  6. Dana-Farber/Harvard Cancer Center (DF/HCC)

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Cyclin-dependent kinase 7 (CDK7) is a central regulator of the cell cycle and gene transcription. However, little is known about its impact on genomic instability and cancer immunity. Using a selective CDK7 inhibitor, YKL-5-124, we demonstrated that CDK7 inhibition predominately disrupts cell-cycle progression and induces DNA replication stress and genome instability in small cell lung cancer (SCLC) while simultaneously triggering immune-response signaling. These tumor-intrinsic events provoke a robust immune surveillance program elicited by T cells, which is further enhanced by the addition of immune-checkpoint blockade. Combining YKL-5-124 with anti-PD-1 offers significant survival benefit in multiple highly aggressive murine models of SCLC, providing a rationale for new combination regimens consisting of CDK7 inhibitors and immunotherapies.

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