CDK12 inactivation across solid tumors: an actionable genetic subtype

Catherine H Marshall; Eddie L Imada; Zhuojun Tang; Luigi Marchionni; Emmanuel S Antonarakis

doi:10.18632/oncoscience.481

CDK12 inactivation across solid tumors: an actionable genetic subtype

Oncoscience. 2019 May 10;6(5-6):312-316. doi: 10.18632/oncoscience.481. eCollection 2019 May.

Authors

Catherine H Marshall^#¹, Eddie L Imada^#², Zhuojun Tang³, Luigi Marchionni³, Emmanuel S Antonarakis¹

Affiliations

¹ Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
² Departamento de Bioquimica e Imunologia, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
³ Sidney Kimmel Comprehensive Cancer Center and Center for Computational Genomics, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.

^# Contributed equally.

Abstract

Inactivating CDK12 alterations have been reported in ovarian and prostate cancers and may have therapeutic implications; however, the prevalence of these mutations across other cancer types is unknown. We searched the cBioPortal and GENIE Project (public release v4.1) databases for cancer types with > 200 sequenced cases, that included patients with metastatic disease, and in which the occurrence of at least monoallelic CDK12 alterations was > 1%. The prevalence of at least monoallelic CDK12 mutations was highest in bladder cancer (3.7%); followed by prostate (3.4%), esophago-gastric (2.1%) and uterine cancers (2.1%). Biallelic CDK12 inactivation was highest in prostate cancer (1.8%), followed by ovarian (1.0%) and bladder cancers (0.5%). These results are the first (to our knowledge) to estimate the prevalence of monoallelic and biallelic CDK12 mutations across multiple cancer types encompassing over 15,000 cases.

Keywords: CDK12; biomarkers; genetics; immunotherapy; prostate cancer.

Abstract

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